ライフサイエンスコーパス: acetylcysteine

1 the phenotype by the antioxidant action of N-acetylcysteine.

2 ss program were blocked by the antioxidant N-acetylcysteine.

3 and can be prevented with the antioxidant N-acetylcysteine.

4 smid that was prevented by the addition of N-acetylcysteine.

5 ine signaling 3), and antioxidants such as N-acetylcysteine.

6 oxide, and these effects were inhibited by N-acetylcysteine.

7 of glutamate, alphaKG, or nucleobases with N-acetylcysteine.

8 ubstantially reduced in mice that received N-acetylcysteine.

9 She was treated with N-acetylcysteine.

10 he NOX subunit NOX2 and by the antioxidant N-acetylcysteine.

11 hronic treatment with the cystine prodrug, N-acetylcysteine.

12 HBEC and did not occur in the presence of N-acetylcysteine.

13 d be partially reversed by the antioxidant N-acetylcysteine.

14 rocesses were reversed by the antioxidant, N-acetylcysteine.

15 vented by the antioxidants glutathione and N-acetylcysteine.

16 ed by capsazepine, and by the antioxidant, N-acetylcysteine.

17 longed therapeutic efficacy as compared to N-acetylcysteine.

18 in uterine arteries, which was blocked by N-acetylcysteine.

19 CD4 T cells is improved by the antioxidant N-acetylcysteine.

20 nit, which was restored in the presence of N-acetylcysteine.

21 88, and oxidative stress was attenuated by N-acetylcysteine.

22 piratory epithelium integrity with EGTA or N-acetylcysteine.

23 diated relaxations, which were reversed by N-acetylcysteine.

24 ure-dependent tone, which were annulled by N-acetylcysteine.

25 other set of mice received the antioxidant N-acetylcysteine.

26 of LKB1 and by incubation with antioxidant N-acetylcysteine.

27 The study drugs (acetylcysteine 1200 mg or matching placebo) were adminis

28 N-acetylcysteine (3.3%) decreased biofilm biomass and kill

29 were observed, as well as increased use of N-acetylcysteine (48.9% vs. 69.3% overall; 15.8% vs. 49.4%

30 steamine bitartrate (60 mg/kg per day) and N-acetylcysteine (60 mg/kg per day) and were assessed ever

31 response system to receive concomitant oral acetylcysteine (600 mg, three times daily) or placebo fo

32 studying the biochemical transformation of N-acetylcysteine, a commonly prescribed Cys supplement dru

33 s performed for several small peptides and N-acetylcysteine, a drug administered intravenously to tre

34 Supplementation of N-acetylcysteine, a glutathione precursor, conferred a pro

35 cell death was rescued in the presence of N-acetylcysteine, a glutathione precursor.

36 gating, and was attenuated by antioxidant N-acetylcysteine, a known scavenger of acrolein.

37 d (2) use the EAAC1(-/-) mouse to evaluate N-acetylcysteine, a membrane-permeable cysteine pro-drug,

38 We posit that treatment with N-acetylcysteine, a precursor of glutathione, the largest

39 Treatment with N-acetylcysteine, a safe prodrug against oxidation, revers

40 Perioperative fenoldopam and N-acetylcysteine abrogate the early postoperative decline

41 urrent administration of the ROS inhibitor N-acetylcysteine abrogated beta-catenin/HIF pathway activi

42 N-acetylcysteine accelerates amputation stump healing in t

43 rug regimen of prednisone, azathioprine, and acetylcysteine; acetylcysteine alone; or placebo.

44 e toxin, whereas replenishing GSH level by N-acetylcysteine administration or activation of nuclear f

45 Mice in posttreatment were treated with N-acetylcysteine after folic acid.

46 JNK inhibitor SP600125, or the antioxidant N-acetylcysteine alleviated insulin resistance, demonstrat

47 rednisone, azathioprine, and acetylcysteine; acetylcysteine alone; or placebo.

48 duced glutamatergic adaptations by chronic N-acetylcysteine also caused enduring inhibition of cocain

49 Furthermore, the administration of N-acetylcysteine also prevented NF-kappaB activation, neut

50 Oral acetylcysteine (also known as N-acetylcysteine) is used

51 ernative antioxidants (vitamin C, DTT, and N-acetylcysteine) also enhanced the chemotactic activity o

52 Chemical chaperones or the antioxidant N-acetylcysteine ameliorated glucose tolerance and insulin

53 Consistently, treatment with anti-oxidant N-acetylcysteine ameliorates muscle necrosis in Stra13-/-

54 t study sought to evaluate the efficacy of N-acetylcysteine amide (NACA) eye drops in reversing the c

55 endothelial (HBMVEC) cells to test whether N-acetylcysteine amide (NACA), a novel antioxidant, preven

56 pothesized that a novel thiol antioxidant, N-acetylcysteine amide (NACA), might ameliorate cellular d

57 N-acetylcysteine amide eye drops were administered beginni

58 peritoneally on postpartum day 10, whereas N-acetylcysteine amide was injected intraperitoneally on p

59 randomly divided into a control group, an N-acetylcysteine amide-only group, a sodium selenite-induc

60 N-acetylcysteine, an amino acid, seems to restore the extr

61 nsible for changes in DICER, we found that N-acetylcysteine, an antioxidant and anti-aldehyde, protec

62 ir, and to pretreatment with antioxidants (N-acetylcysteine and ascorbate) and placebo.

63 effects could be reverted or aggravated by N-acetylcysteine and buthionine sulfoximine, respectively.

64 atment of DCs or CSE with the antioxidants N-acetylcysteine and catalase.

65 he astroglial glutamate transporter GLT-1 (N-acetylcysteine and ceftriaxone) can decrease measures of

66 The antioxidants N-acetylcysteine and glutathione monoethyl ester inhibited

67 om modulation studies of glutathione using N-acetylcysteine and L-buthionine-sulfoximine indicate tha

68 Conversely, antioxidant chemicals (such asN-acetylcysteine and Mn(III)tetrakis(4-benzoic acid)porphy

69 N-acetylcysteine and phosphoinositide 3-kinase (PI3K) inhi

70 s; 133 and 131 patients were enrolled in the acetylcysteine and placebo groups, respectively.

71 All patients received a high dose of N-acetylcysteine and sodium bicarbonate solution.

72 leptogenesis by a transient treatment with N-acetylcysteine and sulforaphane, which act to increase g

73 Four (7%) patients receiving acetylcysteine and three (5%) receiving placebo disconti

74 for the potential roles of bortezomib and N-acetylcysteine, and explore new therapeutic approaches,

75 erior regenerability by each of ascorbate, N-acetylcysteine, and urate when compared to alpha-TOH.

76 In this work, water-dispersible N-acetylcysteine- and l-cysteine-stabilized palladium nano

77 Intravenous sodium bicarbonate and oral acetylcysteine are widely used to prevent acute kidney i

78 /chlorobenzene two-phase system containing N-acetylcysteine as a reducing agent in the aqueous phase.

79 Reactions conducted with ascorbate or N-acetylcysteine as a reductant under aerobic conditions i

80 hase peroxidation system containing excess N-acetylcysteine as a stoichiometric thiol reducing agent

81 suppressor cells, whereas the antioxidant N-acetylcysteine attenuates the inhibitory effects of phen

82 in pre- + posttreatment were treated with N-acetylcysteine before folic acid and after folic acid.

83 e treated with a subcutaneous injection of N-acetylcysteine before the folic acid injection.

84 ylation and activity, whereas antioxidants N-acetylcysteine, beta-naphthoflavone, and tertiary butyl

85 In addition, the potent antioxidant N-acetylcysteine blocked EMT and expression of HIF-1alpha

86 The antioxidant compound N-acetylcysteine blocked the curcumin-induced increased re

87 ation of reactive oxygen species (ROS), as N-acetylcysteine blocked the induction of death receptors

88 New drugs including N-acetylcysteine, bortezomib, recombinant ADAMTS13, and ca

89 rescued by treatment with the antioxidant N-acetylcysteine but not by p53 inactivation.

90 d by the reactive oxygen species scavenger N-acetylcysteine but not by reducing agents or NO pathway

91 It is treated with intravenous acetylcysteine, but the standard regimen is complex and

92 lthough treatable by timely application of N-acetylcysteine, can be fatal.

93 hiols, including cysteine, dithiothreitol, N-acetylcysteine, captopril, bovine and human serum albumi

94 N-Acetylcysteine, catalase, and l-N(G)-monomethyl arginine

95 tudy assessed the safety and tolerability of acetylcysteine combined with pirfenidone in patients wit

96 howed considerably reduced reactivity with N-acetylcysteine compared to the prototypical derivative c

97 Pre-treatment with N-acetylcysteine completely reversed BSO+AUR-induced cell

98 Treatment with N-acetylcysteine could slow the progression of, but not pr

99 itable by pretreating the lymphocytes with N-acetylcysteine, cyclosporin A, or bongkrekic acid, empha

100 Pretreatment with N-acetylcysteine decreases phosphorylation of p53 in citra

101 achieved by infusion of 5% dextrose (during acetylcysteine delivery) or saline (for antiemetic pretr

102 treatment of trichotillomania, found that N-acetylcysteine demonstrated statistically significant re

103 N-Acetylcysteine did not prevent ethanol-induced mortality

104 In this subanalysis, acetylcysteine did not reduce the risk of contrast-induc

105 AK2V617F-mutant cells with the antioxidant N-acetylcysteine diminished reactive oxygen species (ROS),

106 Treatment of mice with the antioxidant N-acetylcysteine diminishes PGC-1alpha variation observed

107 N-acetylcysteine, diphenyleneiodonium, and apocynin blocke

108 ed protection in the context of suboptimal N-acetylcysteine dosing.

109 N-acetylcysteine (dosing range, 1200-2400 mg/d) or placebo

110 N-acetylcysteine (dosing range, 1200-3000 mg/d) or placebo

111 ability of the equine clinical treatments N-acetylcysteine, EDTA, and hydrogen peroxide to disrupt i

112 otosensitivity occurred more frequently with acetylcysteine (eight [13%] patients) than placebo (one

113 The reducing agent N-acetylcysteine eliminated the effects of selenium on ERK

114 emperatures indicate that the -SH group of N-acetylcysteine enhances the rate of its hydrolysis by a

115 mbined with treatment with the antioxidant N-acetylcysteine, establishing that reactive oxygen specie

116 ients with diabetes mellitus included in the Acetylcysteine for Contrast-Induced Nephropathy Trial (A

117 t randomized study evaluating the effects of acetylcysteine for the prevention of contrast-induced ac

118 Treatment with N-acetylcysteine from gestation on normalized most neuroch

119 s: pharmacological (rescue with trolox and N-acetylcysteine), genetic (analysis of metal-sensitive an

120 ctinomycete family produce mycothiol (MSH or acetylcysteine-glucosamine-inositol, AcCys-GlcN-Ins) to

121 61 were assigned to the acetylcysteine group (60 received study medication and i

122 injury (primary end point) was 13.8% in the acetylcysteine group and 14.7% in the control group (rel

123 difference in the change in FVC between the acetylcysteine group and the placebo group (-0.18 liters

124 were no significant differences between the acetylcysteine group and the placebo group in the rates

125 2) and in 114 of 2495 patients (4.6%) in the acetylcysteine group as compared with 112 of 2498 (4.5%)

126 One case of diarrhoea in the acetylcysteine group was considered severe and related t

127 otrusion, and malignant lung neoplasm in the acetylcysteine group, and aortic aneurysm, contusion, fo

128 No adverse events occurred in the N-acetylcysteine group, and N-acetylcysteine was well tole

129 ing EGF-like growth factor and antioxidant N-acetylcysteine had beneficial effects on epithelial woun

130 ltered myocyte properties, the antioxidant N-acetylcysteine had broader effects in limiting glucose o

131 Patients assigned to receive N-acetylcysteine had significantly greater reductions in h

132 Acetylcysteine has been suggested as a beneficial treatm

133 re possible therapeutic approaches include N-acetylcysteine, hypothermia, liver assist devices, and h

134 High-dose antioxidant treatment with N-acetylcysteine improved airspace caliber and attenuated

135 are often steatotic, although addition of N-acetylcysteine improves the quality of the cells obtaine

136 e is controversy regarding the benefits of N-acetylcysteine in acute kidney injury.

137 The NACIAM trial (N-acetylcysteine in Acute Myocardial Infarction) examined

138 letely abolished the protective effects of N-acetylcysteine in Met-KO hepatocytes.

139 The salutary effects of N-acetylcysteine in this mouse model provide an impetus fo

140 ipants (31 randomized to placebo and 35 to N-acetylcysteine) included in the analysis, 59 (89%) were

141 III) tetrakis(4-benzoic acid)porphyrin and N-acetylcysteine increased the ratio of Akt to ERK phospho

142 y addition of nontoxic copper chelators or N-acetylcysteine, indicating a role for copper and reactiv

143 fatty acid beta-oxidation, with S-nitroso-N-acetylcysteine induced site-specific S-nitrosylation of

144 ive stress was blocked by exposing mice to N-acetylcysteine, induction of liver UGT1A1 and CYP2B10 by

145 The cytoprotective antioxidant N-acetylcysteine inhibited Dp44mT-induced autophagosome sy

146 treatment with the free radical scavenger, N-acetylcysteine, inhibited this effect.

147 this study we show that the ROS scavenger N-acetylcysteine inhibits CSR.

148 However, three different N-acetylcysteine interventions neither significantly impro

149 hanism in RYR1-related myopathies and that N-acetylcysteine is a successful treatment modality ex viv

150 ion therapy with cysteamine bitartrate and N-acetylcysteine is associated with delay of isoelectric E

151 bination of oral cysteamine bitartrate and N-acetylcysteine is beneficial for patients with neuronal

152 N-acetylcysteine is more renoprotective than hydration alo

153 Oral acetylcysteine (also known as N-acetylcysteine) is used with pirfenidone to treat idiopa

154 agents (eg, riluzole, ketamine, memantine, N-acetylcysteine, lamotrigine, celecoxib, ondansetron) eit

155 More importantly, the antioxidant, oral N-acetylcysteine led to amelioration of the muscle atrophy

156 tes, reducing reactive oxygen species with N-acetylcysteine lessened protein aggregation and decrease

157 eatment with the redox-active pharmaceutic N-acetylcysteine lowers gastric mucosal neutrophil infiltr

158 N-acetylcysteine may be protective against DILI while taki

159 iously reported that phosphocysteamine and N-acetylcysteine mediate ceroid depletion in cultured cell

160 Timely administration of N-acetylcysteine (N-Ac) prevents the progression of seriou

161 were treated in the presence or absence of N-acetylcysteine (NAC) administered 24 hours and 1 hour be

162 f two structurally unrelated antioxidants: N-acetylcysteine (NAC) and melatonin.

163 probes after pharmacologic challenges with N-acetylcysteine (NAc) and MK-801.

164 ch as glutathione ethyl ester (GSH-EE); or N-acetylcysteine (NAC) attenuate 15d-PGJ(2)-induced platel

165 ent with antioxidants alpha-tocopherol and N-acetylcysteine (NAC) attenuated paraquat-induced implant

166 ntly, it was reported that the antioxidant N-acetylcysteine (NAC) decreased DMXAA-induced TNF-alpha a

167 ng Nkx3.1 mutant mice with the antioxidant N-acetylcysteine (NAC) for 13 weeks post-weaning.

168 N-acetylcysteine (NAC) has anti-atherosclerotic effect wit

169 Systemic N-acetylcysteine (NAC) has been shown to restore glutamate

170 N-acetylcysteine (NAC) has been suggested to prevent relap

171 mbination of prednisone, azathioprine, and N-acetylcysteine (NAC) has been widely used as a treatment

172 N-Acetylcysteine (NAC) has been widely used in cell cultur

173 alities were all rescued by treatment with N-acetylcysteine (NAC) in diabetic females during gestatio

174 N-acetylcysteine (NAC) is an antioxidant with reactive oxy

175 N-acetylcysteine (NAC) is an FDA-approved drug that has lo

176 N-acetylcysteine (NAC) is known to promote endothelial cel

177 The glutathione (GSH) precursor N-acetylcysteine (NAC) is used to treat patients with APAP

178 es, the in vivo effects of the antioxidant N-acetylcysteine (NAC) on two mouse models for NPC1 diseas

179 g administration of the potent antioxidant N-acetylcysteine (NAC) prevented acetaminophen-induced liv

180 estigate whether a donor pretreatment with N-acetylcysteine (NAC) reduces the incidence of DGF in adu

181 ment of HMVEC-d cells with the antioxidant N-acetylcysteine (NAC) significantly inhibited KSHV entry,

182 gers pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) significantly inhibited ROS product

183 ric barrier discharge (DBD) plasma treated N-Acetylcysteine (NAC) solution against planktonic and bio

184 gnificant interaction was observed between N-acetylcysteine (NAC) therapy and rs3750920 within TOLLIP

185 We calibrated and applied an N-acetylcysteine (NAC) thiol reactivity assay as a surroga

186 N-acetylcysteine (NAC) treatment prevents relapse in anima

187 N-acetylcysteine (NAC) was found to improve transplantatio

188 The antioxidant N-acetylcysteine (NAC) was used to decrease ROS in both in

189 ether with 1 of 4 prophylactic regimes (1) N-acetylcysteine (NAC), (2) sodium bicarbonate (NaHCO3) in

190 as to assess the feasibility of using oral N-acetylcysteine (NAC), a glutamatergic modulator and an a

191 In rodents, N-acetylcysteine (NAC), a stimulator of the cystine-glutam

192 N-acetylcysteine (NAC), a thiol-containing antioxidant, ac

193 N-acetylcysteine (NAC), an antidote for acetaminophen pois

194 Furthermore, N-acetylcysteine (NAC), an antioxidant and ROS scavenger,

195 odonium (DPI), a flavoenzyme inhibitor, or N-acetylcysteine (NAC), an antioxidant.

196 N-acetylcysteine (NAC), an FDA-approved anti-mucolytic age

197 zerumbone was abolished by glutathione and N-acetylcysteine (NAC), and this correlated with decreased

198 The only available treatment, N-acetylcysteine (NAC), has a limited time window of effic

199 nto four groups for daily treatment: HBOT, N-acetylcysteine (NAC), HBO and NAC, and control (normoxia

200 stigate the effect of a thiol antioxidant, N-acetylcysteine (NAC), in SSc.

201 sly showed that the glutathione precursor, N-acetylcysteine (NAC), prevented hypoglycemia-associated

202 a total of 10 strategies: saline, statin, N-acetylcysteine (NAC), sodium bicarbonate (NaHCO3), NAC+N

203 ggest that the over-the-counter supplement N-acetylcysteine (NAC), via glutamate modulation in the nu

204 of ISO with the current standard of care, N-acetylcysteine (NAC).

205 lerance, and efficacy of the GSH precursor N-acetylcysteine (NAC).

206 d by the antioxidant L-cysteine derivative N-acetylcysteine (NAC).

207 ndow of the only current treatment option, N-acetylcysteine (NAC).

208 N-Acetylcysteine (NAC, a clinically approved mucolytic dru

209 ions (corticosteroids, pentoxifylline, and N-acetylcysteine [NAC], alone or in combination) with each

210 As compared with placebo, acetylcysteine offered no significant benefit with respe

211 emented HCT 116 cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl o

212 5 non-cancerous cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl s

213 rophy and preserved systolic function with N-acetylcysteine or a placebo for 12 months (n=10 per grou

214 nt of CSE-knockout mice with NaHS, but not N-acetylcysteine or ezetimibe, inhibited the accelerated a

215 macological treatment with the antioxidant N-acetylcysteine or genetic disruption of the DNA damage r

216 rast, reduction of adipose DNA damage with N-acetylcysteine or metformin ameliorated cellular senesce

217 ition of Th17 induction with ROS scavenger N-acetylcysteine or mitoquinone, a specific inhibitor for

218 duced apoptosis was blocked by antioxidant N-acetylcysteine or NF-kappaB inhibitor via down-regulatin

219 nous 0.9% sodium chloride and 5 days of oral acetylcysteine or oral placebo; of these patients, 4993

220 We focused on use of N-acetylcysteine or sodium bicarbonate for the prevention

221 f KB cells with antioxidants vitamin C and N-acetylcysteine or the pharmacological inhibitor PD168393

222 N-Acetylcysteine or tris(2-carboxylethyl)phosphine as co-a

223 lular level, the presence of antioxidants (N-acetylcysteine or vitamin E) significantly reduced the t

224 Administration of an antioxidant chemical, N-acetylcysteine, or ectopically overexpressing a reactive

225 medication (serotonin reuptake inhibitors, N-acetylcysteine, or naltrexone).

226 over intravenous sodium chloride or of oral acetylcysteine over placebo for the prevention of death,

227 f RhoA-deficient mice with a ROS scavenger N-acetylcysteine partially restored thymocyte development.

228 They randomly received N-acetylcysteine, physiologic saline, or sodium bicarbonat

229 he greatest reduction in CIN was seen with N-acetylcysteine plus IV saline in patients receiving LOCM

230 ients receiving LOCM and with statins plus N-acetylcysteine plus IV saline.

231 However, N-acetylcysteine posttreatment worsened folic acid toxicit

232 Glutathione levels did not increase in N-acetylcysteine posttreatment.

233 Glutathione levels decreased less in N-acetylcysteine pretreatment but also increased beginning

234 The survival rates in N-acetylcysteine pretreatment mice were significantly bett

235 N-acetylcysteine pretreatment was effective in reducing th

236 N-acetylcysteine produced these changes by inducing an end

237 Chronic treatment with N-acetylcysteine protects against mitochondrial oxidative

238 Both CV-3988 and N-acetylcysteine reduced MS-WF-stimulated pneumococcal adh

239 Exposure to the antioxidant N-acetylcysteine reduced oxidative stress and improved sur

240 Treating mice in vivo with N-acetylcysteine reduces ROS levels, rescues HSC cycling d

241 red with 71 of 109 allocated to the standard acetylcysteine regimen (adjusted odds ratio 0.26, 97.5%

242 overdose to either the standard intravenous acetylcysteine regimen (duration 20.25 h) or a shorter (

243 with paracetamol poisoning, a 12 h modified acetylcysteine regimen resulted in less vomiting, fewer

244 ve patients assigned to the shorter modified acetylcysteine regimen versus 31 who were allocated to t

245 to confirm the efficacy of the 12 h modified acetylcysteine regimen.

246 We propose that N-acetylcysteine represents the first potential therapeuti

247 traperitoneal injection of the antioxidant N-acetylcysteine rescued defective follicle and oocyte dev

248 urr1 in HEK293T cells, and the antioxidant N-acetylcysteine rescued from this effect.

249 ent of Paf(-/-) mice with the anti-oxidant N-acetylcysteine restored lymphoid progenitor numbers to t

250 Treatment with N-acetylcysteine restored oxidized to total glutathione ra

251 ways of BCR-derived ROS with the scavenger N-acetylcysteine resulted in impaired in vitro BCR-induced

252 tal treatment of mice with the antioxidant N-acetylcysteine reversed the pollutant-induced increased

253 The antioxidant N-acetylcysteine reversed this phenotype, reducing both ba

254 treated with vitamin E or sulforaphane and N-acetylcysteine; samples included A2E-free cells.

255 ld be reduced with either a shorter modified acetylcysteine schedule, antiemetic pretreatment, or bot

256 N-acetylcysteine seems to be beneficial for patients with

257 The antioxidant N-acetylcysteine significantly inhibited ROS generation, A

258 ion (statin therapy, acetylsalicylic acid, N-acetylcysteine, sodium bicarbonate, off-pump coronary re

259 Administration of N-acetylcysteine, sodium bicarbonate, or physiologic salin

260 N-acetylcysteine, sodium bicarbonate, statins, and ascorbi

261 I inhibitor-induced miR-663 expression by N-acetylcysteine suggested that reactive oxygen species (R

262 a more general cytoprotective profile than N-acetylcysteine, suggesting a mechanism of action that is

263 t APAP-induced autophagy was suppressed by N-acetylcysteine, suggesting APAP mitochondrial protein bi

264 e intermediate formed a stable adduct with N-acetylcysteine, suggesting that oxidative transformation

265 ent inflammatory response was inhibited by N-acetylcysteine, suggesting that PRC may contribute to th

266 rsed by its product lactate or antioxidant N-acetylcysteine, suggesting that Y10 phosphorylation-medi

267 on and beta-oxidation products, as well as N-acetylcysteine, taurine and sulfo-conjugates in both rat

268 nophen-induced liver injury at a time when N-acetylcysteine, the standard therapy, has no efficacy.

269 N-Acetylcysteine, theophylline, and other agents have show

270 lesions was abrogated by the anti-oxidant N-acetylcysteine, this treatment did not alter the accumul

271 Fourteen healthy animals were given N-acetylcysteine to evaluate for toxicity and the other 24

272 fected murine macrophages, the addition of N-acetylcysteine to isoniazid treatment potentiated the ki

273 Addition of GSH or N-acetylcysteine to PBMCs selectively restored IL-12 and I

274 the PANORAMA study suggest that addition of acetylcysteine to pirfenidone does not substantially alt

275 cated that clinical benefit from addition of acetylcysteine to pirfenidone is unlikely, with the poss

276 e liver injury indicating need for continued acetylcysteine treatment beyond the standard course (ala

277 r CRH5 but not AB12, MM cells, and in vivo N-acetylcysteine treatment eliminated these effects.

278 Patients who needed intravenous acetylcysteine treatment for paracetamol overdose had ci

279 and May 29, 2014, 1187 patients who required acetylcysteine treatment for paracetamol overdose were r

280 N-acetylcysteine treatment resulted in significant reducti

281 In addition, the N-acetylcysteine treatment significantly increased BKCa ch

282 Compared with placebo, N-acetylcysteine treatment was associated with significant

283 , 217 were assessable 2 h after the start of acetylcysteine treatment.

284 nd demonstrate beneficial effects of early N-acetylcysteine treatment.

285 cal trial of prednisone, azathioprine, and N-acetylcysteine underwent HRCT at study start and finish.

286 patients "much or very much improved" with N-acetylcysteine use compared with 16% taking placebo (P =

287 N-Acetylcysteine use was limited in this group, presumably

288 ain the variation from clinical studies of N-acetylcysteine use.

289 justed rate of decline 125.6 mL/6 months for acetylcysteine vs 34.3 mL/6 months for placebo; differen

290 e adverse event (46 [77%] patients receiving acetylcysteine vs 50 [81%] receiving placebo), adverse e

291 The trial continued as a two-group study (acetylcysteine vs. placebo) without other changes; 133 a

292 The substrate activity of propionyl-s- N-acetylcysteine was found to be negligible and that of n-

293 ccurred in the N-acetylcysteine group, and N-acetylcysteine was well tolerated.

294 n H(2)S-releasing compounds L-cysteine and N-acetylcysteine were added to the cell culture, the amoun

295 d EAAC1(-/-) mice chronically treated with N-acetylcysteine were evaluated at serial time points for

296 15 of the 32 participants (47%) receiving N-acetylcysteine were much or very much improved compared

297 bic acid, caffeic acid, chlorogenic acid and acetylcysteine were screened as antioxidant standards wi

298 dant and redox regulator compounds such as N-acetylcysteine, which could be used preventively in youn

299 rone 4-phenyl butyric acid and antioxidant N-acetylcysteine, which significantly attenuate lewisite-m

300 o interaction between sodium bicarbonate and acetylcysteine with respect to the primary end point (P=