ライフサイエンスコーパス: direct-acting

1 Eradication of hepatitis C virus (HCV) using direct-acting agents (DAA) has been associated with a fi

2 treatments for hepatitis C virus (HCV) using direct-acting agents appear viable, though issues relate

3 ier to drug resistance and are the preferred direct-acting agents to achieve complete sustained virol

4 As with other direct-acting agonists, excitation of the CN neurons occ

5 The assay was evaluated by testing direct-acting and indirect-acting genotoxic compounds wi

6 ring in their hydroxylation patterns against direct-acting and indirect-acting mutagens, namely 4-nit

7 Here, we demonstrate a novel, direct-acting, and synergistic role for 3 hematopoietic

8 aklinza), belong to the most potent class of direct-acting anti-HCV agents described so far, with in

9 onserved LAT intron is unlikely to involve a direct-acting anti-ICP0 antisense mechanism but that the

10 candidates are now receiving treatment with direct-acting anti-viral (DAA) agents that lower the ris

11 r interferon-based dual, triple, or all-oral direct acting antiviral agent therapy, respectively, whe

12 Direct acting antiviral agents (DAA) are highly effectiv

13 alent in the renal transplant population but direct acting antiviral agents (DAA) provide an effectiv

14 l clinical utility in combination with other direct acting antiviral agents.

15 Phase 3 trials of direct acting antiviral drugs (DAAs) for hepatitis C vir

16 ek) and boceprevir (Victrelis) are the first direct-acting antiviral (DAA) agents approved, and many

17 response 12 weeks after therapy (SVR12) with direct-acting antiviral (DAA) agents for recurrent HCV i

18 l benefit from the preclinical evaluation of direct-acting antiviral (DAA) agents in infectious cultu

19 Direct-acting antiviral (DAA) agents will soon revolutio

20 lving from interferon (IFN)-based therapy to direct-acting antiviral (DAA) agents, yet some safety co

21 fe efficacy and tolerance data with all-oral direct-acting antiviral (DAA) combinations in these pati

22 Despite the introduction of direct-acting antiviral (DAA) drugs against hepatitis C

23 the reach and capacity of the VA to deliver direct-acting antiviral (DAA) HCV therapy, supported by

24 us (HCV) variants that are less sensitive to direct-acting antiviral (DAA) inhibitors has not been fu

25 While the current standard of care, a direct-acting antiviral (DAA) protease inhibitor taken i

26 trials in subjects previously treated with a direct-acting antiviral (DAA) regimen.

27 Highly effective direct-acting antiviral (DAA) regimens (90% efficacy) ar

28 py have led to the approval of multiple oral direct-acting antiviral (DAA) regimens by the U.S. Food

29 factors, but their role for IFN-alpha-free, direct-acting antiviral (DAA) regimens is unclear.

30 Direct-acting antiviral (DAA) regimens without IFN are n

31 is C virus (HCV) consists of interferon-free direct-acting antiviral (DAA) regimens, including combin

32 infected chimpanzees during treatment with a direct-acting antiviral (DAA) targeting the HCV NS5b pol

33 BACKGROUND & AIMS: Interferon-free direct-acting antiviral (DAA) therapies are effective in

34 Although direct-acting antiviral (DAA) therapies for chronic hepa

35 The rapid development of direct-acting antiviral (DAA) therapy for HCV infection

36 Direct-acting antiviral (DAA) therapy for hepatitis C vi

37 The efficacy and safety of all-oral direct-acting antiviral (DAA) therapy in HCV-associated

38 Although the recent introduction of direct-acting antiviral (DAA) therapy is extremely encou

39 Direct-acting antiviral (DAA) therapy, recently approved

40 titis C virus-infected individuals receiving direct-acting antiviral (DAA) therapy.

41 Recent introduction of all-oral direct-acting antiviral (DAA) treatment has revolutioniz

42 ed the cost-effectiveness of two alternative direct-acting antiviral (DAA) treatment policies in a re

43 ghly effective and tolerable interferon-free direct-acting antiviral (DAA) treatments could facilitat

44 th the development of new highly efficacious direct-acting antiviral (DAA) treatments for hepatitis C

45 erably with the approval of interferon-free, direct-acting antiviral (DAA)-based combination therapie

46 (HCV) genotype 1-infected patients who fail direct-acting antiviral (DAA)-based regimens remains unk

47 10), protease inhibitor (PI; 2011-2013), and direct-acting antiviral (DAA; 2014-2015).

48 ble future, or until such time that multiple direct-acting antiviral (STAT-C) inhibitors are availabl

49 viral response to a combination regimen of a direct-acting antiviral (telaprevir, an HCV NS3-4A prote

50 BACKGROUND & AIMS: Daclatasvir is a direct-acting antiviral agent and potent inhibitor of NS

51 Daclatasvir is a direct-acting antiviral agent and potent inhibitor of NS

52 c hepatitis C infection, the addition of the direct-acting antiviral agent boceprevir to standard tre

53 The combination of SOF and a second direct-acting antiviral agent is highly effective in TN

54 receiving 12 weeks of SOF along with another direct-acting antiviral agent plus RBV achieved SVR12-9

55 support further evaluation of the three-drug direct-acting antiviral agent regimen of grazoprevir 100

56 atitis C virus (HCV), the combination of the direct-acting antiviral agent telaprevir, pegylated-inte

57 Resumption of direct-acting antiviral agent therapy after a temporary

58 n who had not been treated previously with a direct-acting antiviral agent were assigned randomly to

59 ine-based treatment (using boceprevir as the direct-acting antiviral agent) of those with chronic HCV

60 ty and could help to improve the efficacy of direct-acting antiviral agents (DAA) in the treatment of

61 Recent approval of direct-acting antiviral agents (DAAs) against hepatitis

62 t HCV are now in development, including both direct-acting antiviral agents (DAAs) and host cofactor

63 Currently, direct-acting antiviral agents (DAAs) are evaluated in c

64 Direct-acting antiviral agents (DAAs) are highly effecti

65 Direct-acting antiviral agents (DAAs) are used increasin

66 e (SVR) after treatment with investigational direct-acting antiviral agents (DAAs) has not been exten

67 nse after treatment with regimens containing direct-acting antiviral agents (DAAs) have limited retre

68 actions between antiretroviral drugs and HCV direct-acting antiviral agents (DAAs) must be carefully

69 Direct-acting antiviral agents (DAAs) represent the stan

70 Developments in directed use of new direct-acting antiviral agents (DAAs) to eliminate circu

71 Several new HCV therapies, called direct-acting antiviral agents (DAAs), are available tha

72 improved substantially since the approval of direct-acting antiviral agents (DAAs).

73 al replication, which is the major target of direct-acting antiviral agents (DAAs).

74 resistance-associated variants for all three direct-acting antiviral agents (DAAs); however, in all b

75 iously untreated patients who received three direct-acting antiviral agents (with the ABT-450/r dose

76 V infection could be cured by treatment with direct-acting antiviral agents alone in the absence of i

77 iously untreated patients who received three direct-acting antiviral agents and ribavirin for 8 weeks

78 as designed to evaluate multiple regimens of direct-acting antiviral agents and ribavirin in patients

79 Current therapies with all-oral direct-acting antiviral agents are associated with high

80 Direct-acting antiviral agents are highly efficient trea

81 Survival data with direct-acting antiviral agents are not available.

82 To shorten the course of direct-acting antiviral agents for chronic hepatitis C v

83 ration has recently approved a number of new direct-acting antiviral agents for the treatment of chro

84 Direct-acting antiviral agents have not been studied exc

85 Second generation direct-acting antiviral agents have revolutionized thera

86 Clinical trials of direct-acting antiviral agents in patients chronically i

87 t of hepatitis C virus (HCV) genotype 1 with direct-acting antiviral agents is often accompanied by t

88 virologic response can be achieved with two direct-acting antiviral agents only.

89 azoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents recently approved in the

90 azoprevir (an NS3/4A protease inhibitor) are direct-acting antiviral agents recently approved in the

91 Many other direct-acting antiviral agents representing several clas

92 Direct-acting antiviral agents suppress hepatitis B viru

93 The development of direct-acting antiviral agents that can cure a chronic h

94 It is a challenge to develop direct-acting antiviral agents that target the nonstruct

95 in may benefit from the addition of multiple direct-acting antiviral agents to their treatment regime

96 The development of direct-acting antiviral agents to treat HCV has focused

97 virologic response was achieved when the two direct-acting antiviral agents were combined with pegint

98 l Hepa-C registry who started treatment with direct-acting antiviral agents while awaiting LT were id

99 velopment of new classes of HCV therapy, the direct-acting antiviral agents, also known as specifical

100 With the availability of direct-acting antiviral agents, recently approved therap

101 le data regarding drug-drug interactions for direct-acting antiviral agents, the interactions being t

102 had failed an all-oral regimen of 2 or more direct-acting antiviral agents.

103 essed with new regimens of recently approved direct-acting antiviral agents.

104 sing combination therapies that contain only direct-acting antiviral agents.

105 ng or lacking NS2, to cyclosporine and other direct-acting antiviral agents.

106 aluable insights for combining it with other direct-acting antiviral agents.

107 sight into novel CHC treatments that include direct-acting antiviral agents.

108 ht affect susceptibility to first-generation direct-acting antiviral agents.

109 3 who had failed an all-oral regimen of >/=2 direct-acting antiviral agents.

110 For direct-acting antiviral combinations only weak associati

111 Addition of a third potent direct-acting antiviral drug can reduce the duration of

112 We assessed whether the addition of a third direct-acting antiviral drug to sofosbuvir and ledipasvi

113 All-oral direct-acting antiviral drugs (DAAs) for hepatitis C vir

114 The availability of curative, direct-acting antiviral drugs against hepatitis C virus

115 New direct-acting antiviral drugs for the treatment of chron

116 ase is a prime target for the development of direct-acting antiviral drugs for the treatment of chron

117 Direct-acting antiviral drugs have a high cure rate and

118 w studies have reported the effectiveness of direct-acting antiviral drugs in these patients.

119 assessed the efficacy and safety of the two direct-acting antiviral drugs ombitasvir, an NS5A inhibi

120 e to short-course combination therapies with direct-acting antiviral drugs that might be explored in

121 gy, which has led to development of many new direct-acting antiviral drugs that target key components

122 Sofosbuvir and daclatasvir are direct-acting antiviral drugs used to treat chronic hepa

123 tion, this seems to be less important in the direct-acting antiviral era, when response rates for HCV

124 ponents of treatment, with the addition of a direct-acting antiviral for genotype 1 infection.

125 avirin, with genotype 1 patients receiving a direct-acting antiviral in combination.

126 ssociated with reduced susceptibility to the direct-acting antiviral inhibitor simeprevir.

127 er the elimination of hepatitis C virus with direct-acting antiviral normalizes expression of IFN-sti

128 that birth-cohort screening was followed by direct-acting antiviral plus PEG-IFN+R treatment for tre

129 e treatment) can affect the efficacy of this direct-acting antiviral regimen, and pretreatment resist

130 he once-daily, ribavirin-free, pangenotypic, direct-acting antiviral regimen, glecaprevir coformulate

131 clinical care treatment cohort, treated with direct-acting antiviral regimens between January 1, 2014

132 an ultrarapid virological response on triple direct-acting antiviral regimens by day 2 and received 3

133 No all-oral, direct-acting antiviral regimens have been approved for

134 disease, highly efficacious, well-tolerated, direct-acting antiviral regimens have not been extensive

135 ween race/ethnicity and effectiveness of new direct-acting antiviral regimens in the Veterans Affairs

136 iviral activity of all-oral, ribavirin-free, direct-acting antiviral regimens requires evaluation in

137 In addition, there are now direct-acting antiviral regimens specifically approved f

138 ogression and are less responsive to current direct-acting antiviral regimens than patients infected

139 irologic response after prior treatment with direct-acting antiviral regimens that included the nucle

140 etermine whether more potent interferon-free direct-acting antiviral regimens will allow treatment du

141 atitis C virus with potent, interferon-free, direct-acting antiviral regimens with no activity agains

142 Data outside of clinical trials with direct-acting antiviral regimens with or without ribavir

143 With no available direct-acting antiviral targeting DENV, NS2/NS3 protease

144 Though highly effective direct-acting antiviral therapies are costly, the price

145 Currently available direct-acting antiviral therapies have reduced efficacy

146 Highly effective hepatitis C virus (HCV) direct-acting antiviral therapies that do not require mo

147 nd NS5A are clinically validated targets for direct-acting antiviral therapies.

148 ny of whom cannot attain the new, expensive, direct-acting antiviral therapies.

149 c response (SVR12) during interferon-sparing direct-acting antiviral therapies.

150 d that is relevant to relapses observed with direct-acting antiviral therapies.

151 could have relevance to the success of newer direct-acting antiviral therapies.

152 ers of both humanized mice and patients, and direct-acting antiviral therapy attenuated M2 macrophage

153 Combination direct-acting antiviral therapy of 8-24 weeks is highly

154 arge prospective observational cohort study, direct-acting antiviral therapy with SOF/ledipasvir, omb

155 the efficacy and safety of sofosbuvir-based direct-acting antiviral therapy, individually tailored a

156 changed by the advent of safe and effective direct-acting antiviral therapy, such that most patients

157 Direct-acting antiviral treatment for hepatitis C virus

158 ective salvage therapy for patients for whom direct-acting antiviral treatment has failed.

159 Empirical data on screening and direct-acting antiviral treatment in real-world clinical

160 In clinical trials of interferon-free, direct-acting antiviral treatment of chronic hepatitis C

161 response (SVR) with hepatitis C virus (HCV) direct-acting antiviral-based regimens is commonly assoc

162 ience virologic failure after treatment with direct-acting antiviral-based therapies remains unclear.

163 etreatment of patients who previously failed direct-acting antiviral-based therapies with sofosbuvir-

164 r, daclatasvir, simeprevir, and ribavirin in direct-acting antiviral-experienced patients, as recomme

165 Direct-acting antiviral-mediated clearance of HCV is ass

166 re, Civacir is equally active against tested direct-acting antiviral-resistant HCV isolates in cell c

167 ralization of different HCV genotypes and of direct-acting antiviral-resistant viruses.

168 ded into interferon, protease inhibitor, and direct-acting antiviral.

169 ological response in patients treated with a direct-acting antiviral.

170 s the efficacy and safety of a once-daily, 2-direct-acting-antiviral-agent (2-DAA) combination of sim

171 h sofosbuvir (SOF) in combination with other direct acting antivirals (DAAs) and the antiarrhythmic d

172 All-oral direct acting antivirals (DAAs) have been shown to have

173 nhibitors as combination partners with other direct acting antivirals (DAAs) having a complementary m

174 Combinations of direct acting antivirals (DAAs) that have the potential

175 HCV) treatment, specifically the addition of direct acting antivirals (DAAs), pegylated interferon-al

176 inistered medications that target the virus (direct acting antivirals [DAA]) to pegylated interferon

177 Recent discoveries of direct acting antivirals against Hepatitis C virus (HCV)

178 r prediction after 2 weeks of treatment with direct acting antivirals appears feasible.

179 oral regimens combining different classes of direct-acting antivirals (DAA) are highly effective for

180 The effectiveness of interferon-free direct-acting antivirals (DAA) in treating chronic hepat

181 er sustained virological response (SVR) with direct-acting antivirals (DAA) is unclear.

182 te, prompting a shift toward combinations of direct-acting antivirals (DAA) with the first protease-t

183 ed hepatitis C virus (HCV) patients involves direct-acting antivirals (DAA).

184 Direct-acting antivirals (DAAs) against hepatitis C viru

185 Direct-acting antivirals (DAAs) against Hepatitis C viru

186 n to re-treat patients who do not respond to direct-acting antivirals (DAAs) and the feasibility of f

187 New direct-acting antivirals (DAAs) are being developed and

188 Although several direct-acting antivirals (DAAs) are now available, the t

189 Combinations of direct-acting antivirals (DAAs) can cure hepatitis C vir

190 Several combinations of 2 or 3 direct-acting antivirals (DAAs) can cure hepatitis C vir

191 ants that are resistant to recently approved direct-acting antivirals (DAAs) could be an important cl

192 Direct-acting antivirals (DAAs) effectively eradicate ch

193 ronic hepatitis C virus (HCV) infection with direct-acting antivirals (DAAs) for 6 weeks achieves sus

194 The results from clinical trials testing new direct-acting antivirals (DAAs) for chronic hepatitis C

195 Recent approval of HCV direct-acting antivirals (DAAs) has renewed discussions

196 es has evolved rapidly as safe and effective direct-acting antivirals (DAAs) have become the standard

197 Direct-acting antivirals (DAAs) have changed the landsca

198 Direct-acting antivirals (DAAs) have led to a high cure

199 he immune effects of viral load decline with direct-acting antivirals (DAAs) in blood.

200 Data on IFN-free regimens combining direct-acting antivirals (DAAs) in HCV-associated lympho

201 real-world data on the effectiveness of oral direct-acting antivirals (DAAs) in predominantly minorit

202 Often, availability of all-oral direct-acting antivirals (DAAs) is delayed because of di

203 hortening the duration of treatment with HCV direct-acting antivirals (DAAs) leads to substantial cos

204 Oral direct-acting antivirals (DAAs) represent a major advanc

205 ars after cure of chronic infection with two direct-acting antivirals (DAAs) targeted epitopes in the

206 Most direct-acting antivirals (DAAs) that are being developed

207 strains, there is a pressing need to develop direct-acting antivirals (DAAs) to combat such deadly vi

208 ate resistance of hepatitis C virus (HCV) to direct-acting antivirals (DAAs), due to the small number

209 In the era of direct-acting antivirals (DAAs), it is unclear whether t

210 In the era of highly effective direct-acting antivirals (DAAs), many questions pertaini

211 d on interferon-alpha, ribavirin and the new direct-acting antivirals (DAAs), such as NS3 protease an

212 With the approval of direct-acting antivirals (DAAs), the management of drug-

213 has led to the discovery of new HCV-specific direct-acting antivirals (DAAs), which have an unprecede

214 tients with sustained virologic responses to direct-acting antivirals (DAAs), which lack immunomodula

215 its trajectory with or without scaled-up HCV direct-acting antivirals (DAAs).

216 nce mutations (DRMs) during monotherapy with direct-acting antivirals (DAAs).

217 patitis C virus (HCV) infection treated with direct-acting antivirals (DAAs).

218 viduals, and the potential for resistance to direct-acting antivirals (DAAs).

219 rapies (8-24 weeks) or interferon (IFN)-free direct-acting antivirals (DAAs; 8-12 weeks, 95% sustaine

220 T integrated data from recent trials of oral direct-acting antivirals (SOLAR 1 and 2), the United Net

221 Recent development of direct-acting antivirals against HCV including NS3/4A pr

222 However, the rapid development of direct-acting antivirals against hepatitis C virus will

223 espite the recent success of newly developed direct-acting antivirals against hepatitis C, the diseas

224 eached the market and many others, including direct-acting antivirals and host-targeted agents, are i

225 e discuss the viral proteins targeted by HCV direct-acting antivirals and summarize clinically releva

226 If second-generation direct-acting antivirals are not available, W28 of BOC-b

227 ng that ribavirin complements the effects of direct-acting antivirals as an immunomodulatory compound

228 Treatment with direct-acting antivirals for HCV and wider use of tenofo

229 re-LT versus post-LT HCV treatment with oral direct-acting antivirals for patients with MELD scores b

230 l and subtropical regions, with no available direct-acting antivirals for treatment.

231 The availability of oral direct-acting antivirals has altered the hepatitis C vir

232 atitis C virus (HCV) treatment regimens with direct-acting antivirals have not been extensively studi

233 tes up to 100% when used in combination with direct-acting antivirals having complementary mechanisms

234 The licensing of direct-acting antivirals heralds a new era in the treatm

235 the prevalence of RAVs to currently approved direct-acting antivirals in a large European population

236 is known regarding its effect on response to direct-acting antivirals in interferon-free combinations

237 Studies using direct-acting antivirals in patients with CKD and those

238 The development of direct-acting antivirals in recent years has dramaticall

239 Limited data are available on direct-acting antivirals in the transplant setting for p

240 ge lowers the 50% effective concentration of direct-acting antivirals in vitro, suggesting critical r

241 ment as prevention with highly effective new direct-acting antivirals is a prospective HCV eliminatio

242 rferon-free, guideline-tailored therapy with direct-acting antivirals is highly effective and safe fo

243 ted with HCV transmission and treatment with direct-acting antivirals may prevent further HCV infecti

244 Direct-acting antivirals might overcome factors such as

245 nts in clinical trials with first-generation direct-acting antivirals plus pegylated interferon and r

246 Direct-acting antivirals produce high SVR rates in white

247 th increased treatment uptake and the use of direct-acting antivirals reduced incidence by 77% (from

248 Direct-acting antivirals that suppress HCV replication c

249 Direct-acting antivirals that target nonstructural prote

250 New, simpler therapeutics using direct-acting antivirals that target various stages of t

251 Direct-acting antivirals therapies are now emerging, pro

252 origin of the synergy between interferon and direct-acting antivirals, and facilitates rational treat

253 n interferon-free, ribavirin-free regimen of direct-acting antivirals, comprising daclatasvir (an NS5

254 We assessed the combination of two direct-acting antivirals, ombitasvir (NS5A inhibitor) an

255 ew discusses the potential role for emerging direct-acting antivirals, proposing treatment algorithms

256 vements in the efficacy of HCV therapies via direct-acting antivirals, which also offer reduced treat

257 t affordable triple therapies, including new direct-acting antivirals, will be available starting in

258 of interferon-free, all-oral combinations of direct-acting antivirals.

259 ic sequences in the regions targeted by lead direct-acting antivirals.

260 itis C therapies both involving IFNs and new direct-acting antivirals.

261 that could be used in combination with other direct-acting antivirals.

262 rferon, pegylated-interferon, ribavirin, and direct-acting antivirals.

263 eatment with more complex regimens including direct-acting antivirals.

264 30% fewer treatments are necessary with new direct-acting antivirals.

265 that could be used in combination with other direct-acting antivirals.

266 serve as an attractive target in developing direct-acting antivirals.

267 s global disease despite the availability of direct-acting antivirals.

268 uded increase in treatment uptake and use of direct-acting antivirals.

269 talepsy or analgesia, two typical effects of direct-acting cannabinoid agonists.

270 erivative, SML-10-70-1, which are selective, direct-acting covalent inhibitors of the K-Ras G12C muta

271 These direct-acting drugs allow for simplified and shortened t

272 inhibitors before but not after injection of direct-acting hyperalgesic agents (prostaglandin E2 and

273 similar in magnitude to that induced by the direct-acting hyperalgesic agents but much longer in dur

274 e (DAHP) is considered to be a selective and direct-acting inhibitor of GTP cyclohydrolase I (GTPCH),

275 thyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct-acting monofunctional alkylator.

276 I) hydrolysis and compared it to a number of direct acting muscarinic agonists, two cholinesterase in

277 Compound 5NO2 was found to be a potent direct acting mutagen.

278 BPQ was also found to be a direct-acting mutagen in the Ames test using Salmonella

279 ng PM to NO3/N2O5 resulted in an increase in direct-acting mutagenic activity which was associated wi

280 The direct-acting mutagenicity increased the most after NO3/

281 osterior axis patterning by functioning as a direct-acting nanos mRNA localization factor.

282 By contrast, direct-acting nitroglycerine or prostacyclin improved ce

283 Indeed, only a single direct-acting nos localization factor, Rumpelstiltskin (

284 verge of a new era with the introduction of direct acting oral agents that will transform the treatm

285 ng is not indicated among patients receiving direct-acting oral anticoagulant therapy.

286 , argatroban, bivalirudin, or one of the new direct-acting oral anticoagulants as appropriate.

287 Randomised trials testing direct-acting oral anticoagulants for secondary preventi

288 cific guidance for vitamin K antagonists and direct-acting oral anticoagulants; 4) evaluate whether t

289 e validated with hydrogen peroxide, a simple direct-acting oxidant.

290 CT50547, a direct-acting P2Y12 antagonist, inhibited thrombosis in

291 Ticagrelor is a direct-acting P2Y12 inhibitor and, unlike clopidogrel an

292 Ticagrelor is a direct-acting P2Y12-adenosine diphosphate receptor block

293 The direct-acting platelet P2Y12 receptor antagonist ticagre

294 T1-MMP and MT2-MMP cooperatively function as direct-acting, pro-invasive factors that confer Snail1-t

295 These reports of direct-acting RAS inhibitors provide valuable insight fo

296 ived MT1-MMP, which unexpectedly serves as a direct-acting regulator of macrophage proteolytic activi

297 Ticagrelor is a direct-acting reversibly binding P2Y12 antagonist and is

298 In this article, the discovery of selective, direct acting S1P1 agonists utilizing an ethanolamine sc

299 ry cells and increased responsiveness to the direct-acting stimuli methacholine at 3 and 24 h after e

300 ssue-type plasminogen activator (TPA) with a direct-acting thrombolytic agent, plasmin, in an animal