ライフサイエンスコーパス: APAP

1 APAP administration began at 0 h and continued to 'ALF',

2 APAP and IB were found to interact with proteins involve

3 APAP and IB were found to target vital proteins involved

4 APAP hepatotoxicity-induced liver regeneration involves

5 APAP pretreatment inhibited activation of the early step

6 APAP treatment inhibited complex II activity ex vivo, bu

7 APAP-ALF survivors had significantly lower serum FABP1 l

8 APAP-induced liver toxicity was mirrored by significantl

9 APAP-treated snakes had decreased lymphocyte and increas

10 IU/l vs. 7,585 +/- 5,336 IU/l, p = 0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated m

11 pha (184 +/- 23 vs. 130 +/- 33, p = 0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated m

12 Serum samples from 198 APAP-ALF patients (nested case-control study with 99 sur

13 subset of 121 adults with ALF (including 66 APAP-related patients) had baseline serum samples tested

14 Acetaminophen (APAP) and ibuprofen (IB) are drugs commonly used to alle

15 Acetaminophen (APAP) hepatotoxicity is associated with a high rate of g

16 Acetaminophen (APAP) is a commonly used analgesic responsible for more

17 Acetaminophen (APAP) is a proven lethal oral toxicant in reptiles but t

18 Acetaminophen (APAP) is an effective antipyretic and one of the most co

19 Acetaminophen (APAP) is the active component of many medications used t

20 Acetaminophen (APAP) is the main cause of acute liver failure in the We

21 Acetaminophen (APAP) is widely used as an antifebrile and analgesic dru

22 Acetaminophen (APAP) overdose (APAPo) is predominant in the NIH Pediatr

23 Acetaminophen (APAP) overdose is a frequent cause of drug-induced liver

24 Acetaminophen (APAP) overdose is a major cause of acute liver failure (

25 Acetaminophen (APAP) overdose is one of the leading causes of hepatotox

26 Acetaminophen (APAP) overdose represents the most frequent cause of acu

27 Acetaminophen (APAP) overdoses are of major clinical concern.

28 Acetaminophen (APAP)-induced acute liver failure (ALF) is associated wi

29 Acetaminophen (APAP)-induced acute liver injury (AILI) is a major healt

30 Acetaminophen (APAP)-induced liver injury in humans is associated with

31 Acetaminophen (APAP, paracetamol) poisoning is a leading cause of acute

32 Acetaminophen (APAP; ie, Paracetamol or Tylenol) is generally self-medi

33 on and poor outcomes in acute acetaminophen (APAP)-related liver failure.

34 itical for liver repair after acetaminophen (APAP) overdose.

35 f autophagy protected against acetaminophen (APAP)-induced liver injury in mice by clearing damaged m

36 liver failure (ALF) and in an acetaminophen (APAP)-induced ALF mouse model.

37 patocytes in ALF, and in both acetaminophen (APAP)- and carbon tetrachloride (CCl4)-treated mice.

38 gnaling pathways activated by acetaminophen (APAP) and insulin signaling in hepatocytes with or witho

39 d plasma ALT values following acetaminophen (APAP) exposure in mice.

40 s and patients suffering from acetaminophen (APAP, paracetamol)-induced acute liver failure (ALF) sho

41 abolism-dependent hepatotoxin acetaminophen (APAP) or the direct nephrotoxin cisplatin.

42 he albumin-bound hepatotoxin, acetaminophen (APAP).

43 The diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) reportedly is driv

44 The role of lysosomes in acetaminophen (APAP) hepatotoxicity is poorly understood.

45 me P-450 isoforms involved in acetaminophen (APAP) toxicity were examined in HepaRG cells treated wit

46 In acetaminophen (APAP)- or carbon tetrachloride-induced acute liver injur

47 , and ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate ALF (23%), idi

48 administered a 1:1 mixture of acetaminophen (APAP) and (13)C6-APAP resulted in mass spectra that cont

49 trasensitive determination of acetaminophen (APAP) in the presence of its common interference isoniaz

50 Overdose of acetaminophen (APAP) is the leading cause of acute liver failure (ALF)

51 ntal or intentional misuse of acetaminophen (APAP) is the leading cause of acute liver failure in the

52 ted in the plasma or serum of acetaminophen (APAP) overdose patients.

53 ure 12 h after application of acetaminophen (APAP).

54 ALB/c mice by a toxic dose of acetaminophen (APAP).

55 dney injury in the context of acetaminophen (APAP; paracetamol)-induced liver injury is an important

56 of phospholipase D2 (PLD2) on acetaminophen (APAP)-induced acute liver injury using a PLD2 inhibitor

57 reement with in vivo studies, acetaminophen (APAP) toxicity was most profound in HUVEC mono-cultures;

58 Although necrosis in the acetaminophen (APAP) model is known to be regulated by c-Jun NH2-termin

59 eceptor (PAR)-4 contribute to acetaminophen (APAP)-induced liver damage.

60 coagulopathy in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls.

61 o mediate alcohol- (ALC) and acetaminophen- (APAP) induced toxicity in hepatic and extra-hepatic cell

62 R341H, or R341C in mice predisposes to acute APAP hepatotoxicity, thereby providing direct evidence f

63 poietic cell PAR-4 deficiency did not affect APAP-induced liver injury or plasma TAT levels.

64 nduced liver injury (AILI) without affecting APAP bioactivation and detoxification.

65 xpression but increased JNK activation after APAP administration, which exacerbated APAP-induced live

66 -molecule PUMA inhibitor, administered after APAP treatment, mitigated APAP-induced hepatocyte necros

67 y used drug, its potential application after APAP overdose in patients should be further explored.

68 egulation of proinflammatory cytokines after APAP overdose.

69 faster progression of injury and death after APAP overdose.

70 rtant regulator of macrophage function after APAP overdose.

71 a key regulator of macrophage function after APAP-induced liver injury.

72 2 hrs after APAP injection, the APAP challenged mice were randomized

73 ived macrophages into necrotic lesions after APAP overdose.

74 ocated to mitochondria in mouse livers after APAP treatment followed by mitochondrial protein ubiquit

75 these dynamic functions of macrophages after APAP overdose, however, are not fully understood.

76 occurred in Parkin knock-out (KO) mice after APAP treatment based on electron microscopy analysis and

77 t LC accumulation and higher mortality after APAP overdose compared to ASMase(+/+) littermates.

78 hepatocytes under basal conditions or after APAP and RIPK3(-/-) mice were not protected.

79 and increased hepatocyte proliferation after APAP treatment in their livers compared with WT mice.

80 te, N-acetylcysteine, declines rapidly after APAP ingestion, long before patients are admitted to the

81 ion of compensatory liver regeneration after APAP hepatotoxicity is critical for final recovery, but

82 kinase 3 (GSK3) in liver regeneration after APAP hepatotoxicity using a pharmacological inhibition s

83 gnaling pathways in liver regeneration after APAP overdose and highlighted canonical Wnt signaling as

84 vel role of GSK3 in liver regeneration after APAP overdose and identified GSK3 as a potential therape

85 athways involved in liver regeneration after APAP-induced acute liver injury using a novel incrementa

86 t the mechanisms of liver regeneration after APAP-induced ALF have not been extensively explored yet.

87 c target to improve liver regeneration after APAP-induced ALF.

88 Liver regeneration after APAP-induced liver injury is dose dependent and impaired

89 y the mechanisms of liver regeneration after APAP-induced liver injury, more comprehensive research i

90 t activation of beta-catenin signaling after APAP overdose is associated with timely liver regenerati

91 regeneration is critical for survival after APAP overdose, but the mechanisms remain unclear.

92 ted ASMase(-/-) mice and hepatocytes against APAP hepatotoxicity, effects that were reversed by chlor

93 MB can effectively protect mice against APAP-induced liver injury by bypassing the NAPQI-altered

94 cal PKC inhibitor (Go6976) protected against APAP by inhibiting JNK activation.

95 ors from mitochondria, and protected against APAP-induced hepatocyte necrosis and liver injury in mic

96 s, and Parkin KO mice were protected against APAP-induced liver injury compared with wild type mice.

97 kin-mediated mitophagy in protection against APAP-induced liver injury.

98 P treatment, resulting in protection against APAP-mediated hepatic insulin resistance and alterations

99 ternative electron carrier, protects against APAP-induced hepatocyte injury.

100 essential for NAC-mediated recovery against APAP-induced hepatotoxicity.

101 ating monocyte-derived macrophages aggravate APAP hepatotoxicity, and the pharmacological inhibition

102 Further, both exosomes- and ALC/APAP-induced toxicity was reduced/abolished by a selecti

103 atic (monocytic) cells with exosomes +/- ALC/APAP.

104 rinking animal model and their effect on ALC/APAP-induced toxicity in monocytic cells.

105 These findings suggest that ALC/APAP-induced toxicity in the presence of exosomes are me

106 , CO gas inhalation significantly alleviated APAP-induced liver damage in vivo and correspondingly re

107 duced by overdose of N-acetyl-p-aminophenol (APAP) and defined three distinct MF subsets that populat

108 d by acetaminophen (acetyl-para-aminophenol [APAP]) is the main cause of acute liver failure and live

109 Acetaminophen (N-acetyl-p-aminophenol, APAP) and (13)C6-APAP were incubated with rat liver micr

110 Acetaminophen (N-acetyl-para-aminophenol; APAP) overdose is the most common cause of acute liver f

111 ing CYP2E1 cargo further exacerbate ALC- and APAP-induced toxicity in both hepatic and monocytic cell

112 plasma exosomal CYP2E1 in mediating ALC- and APAP-induced toxicity.

113 of exosomal CYP2E1 in exacerbating ALC- and APAP-induced toxicity.

114 onist inhibited APAP induced hypothermia and APAP was without effect on body temperature in Trpa1(-/-

115 icriviroc) reduces monocyte infiltration and APAP-induced liver injury (AILI) in mice.

116 without (N = 27) organ injury (APAP-TOX and APAP-no TOX, respectively).

117 Livers from control mice given VPA and APAP accumulated cholesterol in the mitochondria and had

118 The combination of VPA and APAP increased expression of CYP2E1, formation of NAPQI-

119 ere resistant to induction of ALF by VPA and APAP, despite increased mitochondrial levels of glutathi

120 toxicity following administration of VPA and APAP.

121 elop ALF following administration of VPA and APAP.

122 lcysteine to control mice prevented VPA- and APAP-induced ER stress and liver injury.

123 Patients with ALF as well as APAP-treated mice displayed increased ferritin and dimin

124 2G7 treatments significantly attenuated APAP-induced serum elevations of alanine aminotransferas

125 r microsomes, which are known to bioactivate APAP to the reactive metabolite N-acetyl-p-benzoquinone

126 t in the treatment of liver damage caused by APAP.

127 -ol rescues mice from liver injury caused by APAP.

128 Whereas direct toxicity exerted by APAP metabolites is a key determinant for early hepatocy

129 Bcl-2 family member, was markedly induced by APAP in mouse livers and in isolated human and mouse hep

130 PUMA induction by APAP was p53 independent, and required receptor-interact

131 talk between signaling pathways triggered by APAP and insulin signaling in hepatocytes, which is in p

132 1 mixture of acetaminophen (APAP) and (13)C6-APAP resulted in mass spectra that contained "twin" ions

133 en (N-acetyl-p-aminophenol, APAP) and (13)C6-APAP were incubated with rat liver microsomes, which are

134 pathways were modulated in mice with chronic APAP treatment, resulting in protection against APAP-med

135 miRNA classifier model accurately diagnosed APAP-TOX in the test cohort.

136 However, direct APAP hepatoxicity and liver injury at early times post-A

137 lation during NAC treatment can discriminate APAP hepatotoxicity from ischemic hepatitis.

138 retic non-steroidal anti-inflammatory drugs, APAP elicits hypothermia in addition to its antipyretic

139 eased and prolonged JNK activation; elevated APAP protein adducts; K8 hyperphosphorylation at S74/S43

140 ls (HIF-2alpha(mye/-) ) markedly exacerbated APAP-induced liver injury (AILI) without affecting APAP

141 after APAP administration, which exacerbated APAP-induced liver injury.

142 hepcidin decreases early during experimental APAP-induced ALF, is an independent predictor and might

143 Upon experimental APAP overdose in mice, monocyte-derived macrophages (MoM

144 represent a promising therapeutic agent for APAP-induced liver injury.

145 y histology and immunohistochemistry and for APAP metabolism, endoplasmic reticulum (ER) stress, and

146 help identify future therapeutic targets for APAP-induced hepatotoxicity.

147 c insights and novel therapeutic targets for APAP-induced liver injury.

148 ential target for regenerative therapies for APAP-induced acute liver failure.

149 to develop novel regenerative therapies for APAP-induced acute liver failure.

150 -/-) hepatocytes display lower threshold for APAP-induced cell death and defective fusion of mitochon

151 ing hits, 2) overlap of expression data from APAP overdose studies, and 3) predicted affected biologi

152 monocyte-derived macrophages, isolated from APAP-treated mice, with necrotic hepatocytes decreased e

153 knockout mice, which were not protected from APAP.

154 ations in fasted Stard1(DeltaHep) mice given APAP alone.

155 ere significantly older, less likely to have APAP overdose, and had a lower overall 3-week survival c

156 d lysosomal cholesterol (LC) accumulation in APAP hepatotoxicity.

157 The proximate cause of death in APAP-treated snakes was likely acute methemoglobinemia a

158 No differences in APAP serum levels, glutathione, or adenosine triphosphat

159 y, the data suggest that miRNA elevations in APAP toxicity represent a regulatory response to modify

160 the role of reactive metabolite formation in APAP-induced chemical stress, both the hepatotoxicity an

161 al signaling and apoptosis in hepatocytes in APAP liver disease.

162 types of immune cells are also implicated in APAP-induced liver injury.

163 bution of sterile postinjury inflammation in APAP-induced acute liver injury (APAP-ALI) and justifies

164 onfirmed that necroptosis is not involved in APAP toxicity by using mixed lineage kinase domain-like

165 tematically identify novel genes involved in APAP-induced hepatotoxicity and to provide potential tar

166 9)/JNK phosphorylation is mainly involved in APAP-induced liver injury.

167 d therapeutic window, as compared to NAC, in APAP-ALI.

168 es in oxygen carrying capacity were noted in APAP-treated snakes indicated by a 50-60% increase in me

169 n-driven platelet activation participates in APAP hepatotoxicity.

170 RIPK1 participates in APAP-induced necrosis upstream of JNK activation whereas

171 ticularly autophagy, play a critical role in APAP cytotoxicity.

172 hepatocyte necrosis plays a critical role in APAP-induced liver injury (AILI).

173 on of FABP1 as a clinical prediction tool in APAP-ALF warrants further investigation.

174 ute liver injury after any insult, including APAP overdose, is followed by compensatory liver regener

175 xtraction by 25-hydroxycholesterol increased APAP-mediated mitophagy and protected ASMase(-/-) mice a

176 In contrast, a TRPA1 antagonist inhibited APAP induced hypothermia and APAP was without effect on

177 er recovery from acute toxic liver injuries (APAP and carbon tetrachloride) by increasing tumour necr

178 ammation in APAP-induced acute liver injury (APAP-ALI) and justifies development of anti-inflammatory

179 (N = 27) and without (N = 27) organ injury (APAP-TOX and APAP-no TOX, respectively).

180 Interestingly, APAP induced translocation of RIPK1 to mitochondria, whi

181 ales were injected i.p. with 50 or 250 mg/kg APAP or phosphate-buffered saline on gestation day 12.5;

182 T cells significantly increased on 250 mg/kg APAP.

183 4 and 18 hours after injection of 300 mg/kg APAP.

184 The effects of a lethal APAP oral dose on methemoglobin (MetHb, non-oxygen carry

185 cted localised bioluminescence in the liver (APAP) and kidneys (cisplatin) in vivo and ex vivo, whils

186 ation of STARD1 following ER stress mediates APAP hepatoxicity via SH3BP5 and phosphorylation of JNK1

187 We conclude that TRPA1 mediates APAP evoked hypothermia.

188 administered after APAP treatment, mitigated APAP-induced hepatocyte necrosis and liver injury.

189 -Cas9 gene knockouts were treated with 15 mM APAP for 30 minutes to 4 days.

190 using an AMPK activator oppositely modulated APAP cytotoxicity, suggesting that p-AMPK and AMPK regul

191 re not detected in control spectra (i.e., no APAP administered).

192 responsible for the hypothermic activity of APAP.

193 eous, but not intrathecal, administration of APAP elicited a dose dependent decrease in body temperat

194 of yeast induced pyrexia, administration of APAP evoked a marked hypothermia in wildtype and Trpv1(-

195 ministration of VPA before administration of APAP increased the severity of liver damage in control m

196 eneration was not secondary to alteration of APAP-induced hepatotoxicity, which remained unchanged af

197 an clock in modulating the chronotoxicity of APAP, we used a conditional null allele of brain and mus

198 In a cohort of APAP overdose patients (N = 74) with and without establi

199 candidate for the accurate determination of APAP and INH within human fluids and pharmaceutical form

200 An orally-ingested lethal dose of APAP appears to be a humane method for lethal control of

201 tarting from 4 hours after 600 mg/kg dose of APAP, resulted in early initiation of liver regeneration

202 Our aim was to identify the effects of APAP in pregnancy using a mouse model.

203 Consistent with the toxic effects of APAP in the liver and cisplatin in the kidney, immunohis

204 ere less susceptible to the toxic effects of APAP, including parameters of oxidative stress and ATP d

205 se inhibitor that ameliorates the effects of APAP-induced acute liver failure in the mouse and theref

206 ase (JNK) mediate the hepatotoxic effects of APAP.

207 of characteristic spatiotemporal features of APAP hepatotoxicity within hepatic lobules.

208 The direct hepatotoxicity of APAP triggers a cascade of innate immune responses that

209 500 mg/kg of APAP challenge caused acute liver damage.

210 Mice were injected with 600 mg/kg of APAP or underwent bile duct ligation (BDL).

211 oRNA-122 and completely abrogated markers of APAP-induced inflammation (tumor necrosis factor, monocy

212 However, the mechanisms of APAP-induced necrosis and liver injury are not fully und

213 nd that the reactive oxidative metabolite of APAP, N-acetyl-p-benzoquinoneimine (NAPQI), caused the s

214 a indicate that all the major metabolites of APAP and multiple low-abundance metabolites (e.g., aceta

215 te liver regeneration in the murine model of APAP induced liver injury, which was associated with a m

216 Using various strategies in a mouse model of APAP overdose, the authors demonstrate that platelets pa

217 dy treatment improves survival in a model of APAP-ALI.

218 ers are higher in serum from nonsurvivors of APAP-induced ALF (AALF), compared to survivors.

219 at recommended doses, whereas an overdose of APAP can cause severe liver damage.

220 y of hepatocytes driving the pathogenesis of APAP-induced acute liver injury, and PLD2 may therefore

221 ll known, those that halt the progression of APAP liver disease and facilitate liver recovery are les

222 The electroanalytical sensing of APAP and INH are possible with accessible linear ranges

223 iO-SPEs were evaluated toward the sensing of APAP and INH in human serum, urine, saliva, and tablet s

224 ctrocatalytic activity toward the sensing of APAP and INH with an enhanced analytical signal (voltamm

225 e ability of VPA to increase the severity of APAP-induced liver damage was observed in FRGN mice with

226 antidote N-acetylcysteine (NAC) treatment of APAP-induced liver injury in wild-type mice, the liver i

227 our in vivo data suggest that chronic use of APAP may be associated with insulin resistance in the li

228 s study was to evaluate the effects of CO on APAP-induced hepatotoxicity and CO's relationship to reg

229 e found that the protective effects of CO on APAP-induced liver damage were mediated by down-regulati

230 em cells in the fetal liver were observed on APAP treatment.

231 nd the mitophagy regulator protein Parkin on APAP-induced expression of the ER stress-associated apop

232 For years, research on APAP overdose has been focused on investigating the mech

233 e administration of CAY10594 at 6 hours post APAP challenge.

234 ome than serum creatinine concentration post-APAP overdose.

235 y exert proinflammatory functions early post-APAP, thereby aggravating liver injury.

236 infiltrate liver as early as 8-12 hours post-APAP overdose and form dense cellular clusters around ne

237 f monocytes and attenuated liver injury post-APAP overdose at early time points.

238 (mye/-) mice compared to wild-type mice post-APAP challenge.

239 (10 mg/kg, IP, administered 90 minutes post-APAP) protected against hepatotoxicity, whereas mice tre

240 prognostic biomarker of patient outcome post-APAP overdose.

241 oxicity and liver injury at early times post-APAP overdose were unaffected by syndecan-1, suggesting

242 and is elevated in clinical and preclinical APAP-ALI.

243 ified its mechanism of action in preclinical APAP-ALI.

244 arison with h2G7 in vitro and in preclinical APAP-ALI.

245 udies reveal an association between prenatal APAP use and an increased risk for asthma.

246 r data provide strong evidence that prenatal APAP interferes with maternal immune and endocrine adapt

247 on and hepatic platelet accumulation promote APAP-induced liver injury, independent of platelet PAR-4

248 nti-CD41 antibody also significantly reduced APAP-mediated liver injury and thrombin generation, indi

249 of the hepatocyte clock dramatically reduces APAP bioactivation and toxicity in vivo and in vitro bec

250 By a manual search for all reported APAP metabolite ions, no additional twin-ion signals wer

251 151a-3p and miR-382-5p specifically reported APAP toxicity - being unaffected by drug-induced kidney

252 is dose dependent and impaired after severe APAP overdose.

253 rmic activity was independent of TRPV1 since APAP evoked hypothermia was identical in wildtype and Tr

254 be potentially modulated even in late-stage APAP-induced acute liver failure.

255 PUMA deficiency suppressed APAP-induced mitochondrial dysfunction and release of ce

256 The data demonstrate that APAP treatment leads to HIF-2alpha stabilization in hepa

257 Here, we found that APAP overdose in mice caused liver damage accompanied by

258 In-vitro studies found that APAP protein adducts were increased at 1 h, followed by

259 We observed that APAP challenge caused stabilization of hypoxia-inducible

260 Here we show that APAP interferes with the formation of mitochondrial resp

261 Numerous studies have shown that APAP hepatotoxicity in mice involves mitochondrial dysfu

262 cantly attenuated liver damage caused by the APAP challenge, eliciting an enhanced survival rate.

263 -3beta (Serine 9)/JNK phosphorylation in the APAP-induced acute liver injury model.

264 2 hrs after APAP injection, the APAP challenged mice were randomized to receive treatmen

265 leviating acute hepatotoxicity attributed to APAP overdose.

266 ting that necroptosis does not contribute to APAP-induced necrosis and RIPK1 has a unique, independen

267 Mitochondrial dysfunction contributes to APAP-induced liver injury but the mechanism by which APA

268 le data points), 9 doublets corresponding to APAP metabolites were identified.

269 susceptibility of ASMase(-/-) hepatocytes to APAP and the impairment in the formation of mitochondria

270 ferase (NNMT) levels and were predisposed to APAP-induced hepatotoxicity.

271 This resistance to APAP is also observed in a primary human hepatocyte (PHH

272 ic deletion of FcRn results in resistance to APAP-induced liver injury through increased albumin loss

273 own of Parkin have differential responses to APAP-induced mitophagy and liver injury in mice.

274 transplantation restored the sensitivity to APAP in a GPBAR1-dependent manner.

275 rug-mediated ASMase disruption sensitizes to APAP-induced liver injury.

276 of nonhematopoietic cell PAR-4 signaling to APAP hepatotoxicity.

277 LC accumulation determines susceptibility to APAP hepatotoxicity by modulating mitophagy, and imply t

278 ed mitophagy and increased susceptibility to APAP.

279 tective against, or cause susceptibility to, APAP-induced liver injury.

280 ng anti-HMGB1 neutralizing antibody to treat APAP overdose for 24-48 hours.

281 f HMGB1-specific therapy as a means to treat APAP-ALI and other inflammatory conditions.

282 Although mechanisms that trigger APAP-induced liver injury (AILI) are well known, those t

283 The molecular mechanisms underlying APAP-induced liver damage remain incompletely understood

284 o unopposed progression of liver injury upon APAP overdose.

285 33, p = 0.0086), APAP-alone-treated mice vs. APAP + neostigmine-treated mice) and histopathological s

286 /l, p = 0.0013), APAP-alone-treated mice vs. APAP + neostigmine-treated mice), inflammatory cytokine

287 uced liver injury but the mechanism by which APAP causes hepatocyte toxicity is not completely unders

288 -administered mice which are challenged with APAP.

289 Serum samples of children with APAP overdose had significant elevation of miR-122-5p, m

290 Compared with APAP-treated wild-type mice, biomarkers of hepatocellula

291 ed and 46 were 3-fold or more decreased with APAP-TOX.

292 ignificantly decreased in dams injected with APAP, accompanied by a morphologically altered placenta.

293 f intracellular ATP without interfering with APAP bioactivation.

294 In patients with APAP-ALF, FABP1 may have good potential to discriminate

295 y were examined in HepaRG cells treated with APAP (20 mM).

296 Subsequently, control mice were treated with APAP (350 mg/kg) followed by the beta-adrenoceptor agoni

297 In male C57BL/6J mice treated with APAP (450 mg/kg, intraperitoneally [IP]), MB (10 mg/kg,

298 HC-specific HMGB1-null HC were treated with APAP + NAC.

299 st hepatotoxicity, whereas mice treated with APAP alone developed massive centrilobular necrosis and

300 TP1B-deficient mice chronically treated with APAP.

301 +2(DeltaHep)) were given VPA with or without APAP.