ライフサイエンスコーパス: CCl4

1 CCl4 caused similar acute liver injury in mutant and wil

2 CCl4 effects on cholangiocytes were reversed by day 28.

3 CCl4 increased the binding of ryanodine, a specific liga

4 CCl4 induces steatosis by enhancing proteasomal degradat

5 CCl4 or 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)

6 CCl4 produced similar fibrosis and necroinflammation and

7 CCl4 treatment causes a decrease in large duct mass as a

8 CCl4 treatment enhances degeneration and DNA damage in N

9 CCl4-gavaged mice were also injected with attenuated ade

10 K), whereas the thermodynamic stability of 1:CCl4 complex was -2.7 kcal/mol (DeltaGdegrees, 298 K).

11 CYP2E1 levels nor covalent binding of [14C] CCl4-derived radio-label differed between the groups, su

12 We used a fast food diet (FFD) and a CCl4 micro dose (0.5 ml/kg B.wt) for 8 weeks in Wistar r

13 tive, 1-fluoro-2-isocyanato-ethane (1), in a CCl4 solution at room temperature.

14 Here, using a CCl4-induced rat model of irreversible and fatal hepatic

15 and AFP gene expression was ranked as 2-AAF/ CCl4 > or = 2-AAF/PHx > 2-AAF/AA.

16 Using the protocols of 2-AAF/ CCl4 and 2-AAF/PHx, when DAPM was given 24 hours before

17 response with the above two protocols (2-AAF/CCl4 and 2-AAF/PHx) as affected by previous bile ductula

18 helia was seen with 2-AAF/AA than with 2-AAF/CCl4.

19 Furthermore, an AAF/CCl4-mediated increase in DR and fibrosis were attenuate

20 phagy-lysosome pathway was essential for AAF/CCl4-induced DR-fibrosis.

21 Haploinsufficiency of Gata4 accelerated CCl4 -induced liver fibrosis in adult mice.

22 Acute CCl4 -mediated liver injury in WT mice induced endogenou

23 d liver injury and proliferation after acute CCl4 treatments.

24 We report that acute CCl4 administration to WT mice resulted in early ER stre

25 After CCl4 treatments, TERT, C/EBPalpha and FXR are repressed

26 lated UCP-2 throughout the time course after CCl4 administration, leading to sustained inhibition of

27 Two days after CCl4 administration, there was an increased number of sm

28 on was essentially completed by 4 days after CCl4 injection, but replication at a low level persisted

29 retin-stimulated cAMP synthesis 2 days after CCl4 treatment.

30 mice were more susceptible to fibrosis after CCl4 administration (37% increase in collagen staining).

31 ortality in steatotic rats 12-72 hours after CCl4 administration, whereas all nonsteatotic rats survi

32 ntrilobular hepatocytes 10 to 48 hours after CCl4 exposure.

33 STAT3 binding during the first 5 hours after CCl4, high plasma TNF, and reduced levels of plasma inte

34 ich signaling is known to be increased after CCl4 exposure in the liver.

35 were inhibited in the steatotic livers after CCl4 administration and led to progressive expansion of

36 minished in the liver of STAT1-/- mice after CCl4 administration compared to wild-type mice.

37 2F1 complexes in C/EBPalpha-S193D mice after CCl4 treatments.

38 ectable (<5 pg/ml) to 185 +/- 30 pg/ml after CCl4, a 37-fold increase.

39 duced after bile duct ligation but not after CCl4-induced cirrhosis, we examined NOS activity and nit

40 for the increased liver proliferation after CCl4 treatments and for development of drug-mediated liv

41 nd acceleration of liver proliferation after CCl4 treatments.

42 g liver tissue damage and regeneration after CCl4 intoxication.

43 R-1 inhibited hepatocyte DNA synthesis after CCl4 injection.

44 SRSF3 protects mice against CCl4 -induced fibrosis and carcinogenesis and suppresses

45 with high amounts of phenolics (SP2) against CCl4-induced acute hepatotoxicity were evaluated in rats

46 phage and/or neutrophil depletion aggravated CCl4 -induced liver injury and impeded liver regeneratio

47 B022 protected against not only NIK but also CCl4-induced liver inflammation and injury.

48 2 < 7 < 13 < 8 < 14 congruent with 19-21 and CCl4 < dioxane < MeCN < t-BuOH < MeCN:phosphate buffer (

49 ression was also examined in an acute AA and CCl4 injury.

50 osis and both in mouse bileductligation- and CCl4 -induced fibrosis.

51 PCM calculations (with H2O, CH2Cl2, and CCl4 as model solvents) were employed to examine solvati

52 combination of diethylnitrosamine (DEN) and CCl4, along with either LPS or E. coli infection.

53 mixed solvent of the benzene derivative and CCl4.

54 using a two-phase box consisting of H2O and CCl4 to mimic the micellar environment utilized in the 1

55 differences in base associations in H2O and CCl4.

56 ne), and the mixed solvent of mesitylene and CCl4 (0.83 mole fraction CCl4), are used to study solute

57 d choline-deficient diet-fed db/db mice, and CCl4 -induced fibrosis in rats).

58 partial portal vein ligation (PVL) model and CCl4-induced cirrhosis.

59 olium hexafluorophosphate ([C4MIM][PF6]) and CCl4 were used as an extractant and dispersant solvent,

60 e oxidative stress, such as sodium arsenite, CCl4, lipopolysaccharide (LPS), or tumor necrosis factor

61 m-1 in non-hydrogen bonding solvents such as CCl4, near 1650 cm-1 in aqueous solution, and near 1610

62 iding hazardous chlorinated solvents such as CCl4.

63 occur after exposure to hepatotoxins such as CCl4.

64 hat selectively probe molecular structure at CCl4/H2O and hydrocarbon/H2O interfaces show that the hy

65 netic deletion of PARP-1 markedly attenuated CCl4 -induced hepatocyte death, inflammation, and fibros

66 vivo delivery of Ad-Adn markedly attenuates CCl4-induced expression of key integrin proteins and mar

67 sis was induced by bile duct ligation (BDL), CCl4 intoxication, thioacetamide intoxication or continu

68 Cirrhotic (bile duct ligation/BDL; CCl4 intoxication) and non-cirrhotic (partial portal vei

69 Injection of IL-6 30 minutes before CCl4 administration corrected the deficiency of hepatocy

70 ) kinetics of phenol to benzene in a benzene/CCl4 mixture is investigated.

71 nodine receptor; ruthenium red did not block CCl4 metabolism to CCl3.

72 cally different reference standards for both CCl4 and CHCl3 (two of each).

73 ppears to be very sensitive to activation by CCl4 as effective concentrations (e.g., 50 microM) did n

74 way at 12 hours after acute insult caused by CCl4 administration, as well as a 23% decrease in GSH co

75 ansferase levels, the acute injury caused by CCl4 appeared to be similar in the three groups of anima

76 (51D) attenuated hepatocyte damage caused by CCl4, TGF-beta1, and chemokine production.

77 ore, toxic injury to cultured hepatocytes by CCl4 resulted in release of cytosolic beta-glucosidase i

78 the hepatocyte mitogenic response induced by CCl4 injury in mouse liver.

79 educed bridging fibrosis that was induced by CCl4 or DDC.

80 Upon chronic liver damage induced by CCl4 or methionine-choline-deficient (MCD) diet, liver i

81 two liver cirrhosis mouse models induced by CCl4 or thioacetamide, we showed that targeting AR in th

82 to mice attenuates liver fibrosis induced by CCl4 treatment or bile duct ligation.

83 of a series of phenols in CCl4 and 1% CD3CN/CCl4 provide relative acidities.

84 omy or administration of damaging chemicals (CCl4 , acetaminophen, etc.).

85 of ionic liquid (IL), carbon tetra chloride (CCl4) and sonication time (St).

86 To test this, we performed acute or chronic CCl4 administration to WT and IRF3-, Toll/Interleukin-1R

87 death and fibrosis both in acute or chronic CCl4 In contrast, mice deficient in type I IFN receptors

88 Interestingly, the chronic CCl4 -induced liver injury was also characterized by mit

89 ve an impact on liver pathology, we compared CCl4-induced fibrosis development in B cell-deficient an

90 onalcoholic steatohepatitis (NASH) comprised CCl4 -treated and high-fat, high-carbohydrate diet-fed S

91 ution in the reactive, strongly coordinating CCl4 solution and in the inert, weakly coordinating hexa

92 as no differences were observed between CTRL+CCl4 and HFD+CCl4 mice.

93 hibited hepatoprotective effects against DEN/CCl4-induced injury by reducing DCLK1 expression and imp

94 laminofluorene (2-AAF)/hepatic injury (i.e., CCl4, partial hepatectomy [PHx]) protocol.

95 propyl sulfone (6) is unreactive with either CCl4 or CBrCl3 in KOH-t-BuOH, its phenoxide anion strong

96 The serum biochemical profile of the FFD-CCl4 model showed an increase in liver injury and fibros

97 sis, steatohepatitis and fibrosis in the FFD-CCl4 model when compared to the individual effects of a

98 In summary, we find that the FFD-CCl4 rat model developed NAFLD histological features inc

99 nistration of plerixafor and G-CSF following CCl4 resulted in 87% survival (n = 8, P < 0.05).

100 iver, but its expression decreases following CCl4 injection.

101 detected in the circulation, even following CCl4 administration, which we hypothesized might be expl

102 d approximately three- to fourfold following CCl4-induced oxidative stress or treatment with the DNA-

103 of p21 in pericentral hepatocytes following CCl4 injection contributes to subsequent necrosis.

104 Hepatocyte proliferation following CCl4 treatment was also reduced in anti-TNF-alpha antibo

105 ositively modulates liver recovery following CCl4 exposure presumably by stimulating early-immediate

106 rmore, the emission distribution derived for CCl4 throughout the United States is more consistent wit

107 Likewise, the activation free energy for CCl4 departing the basket was found to be 13.1 kcal/mol

108 The lag period for CCl4-induced release of calcium was associated with the

109 these levels of CCl4, and the lag period for CCl4-induced release of calcium was shorter under anaero

110 t of mesitylene and CCl4 (0.83 mole fraction CCl4), are used to study solute-solvent dynamics via obs

111 f the COL1A2 promoter in stellate cells from CCl4-treated mice and repression of such activation by A

112 ree reference quinoline-based compounds from CCl4 solutions onto a polycrystalline platinum surface w

113 hesis was examined in FSC lines derived from CCl4-induced cirrhotic rat liver (cirrhotic FSCs) and no

114 ere also reduced in primary hepatocytes from CCl4-treated KO mice.

115 erminally diseased hepatocytes isolated from CCl4-treated rats; and rapidly reversed fatal liver fail

116 In livers from CCl4 and BDL-cirrhotic terutroban-treated rats, endothel

117 ave combined effects in protecting mice from CCl4- and acetaminophen-induced liver injury.

118 inally, S1PR2 inhibition protected mice from CCl4-induced liver fibrosis.

119 DNA) failed to increase during recovery from CCl4 exposure.

120 both methods and laboratories, samples from CCl4 and CHCl3 degradation experiments were analyzed and

121 hepatotoxic agents, such as d-galactosamine, CCl4, and thioacetamide, were also ineffective in induci

122 nual average US emission of 4.0 (2.0-6.5) Gg CCl4 y(-1) during 2008-2012, which is almost two orders

123 0.06 Gg y(-1)) but only 8% (3-22%) of global CCl4 emissions during these years.

124 d collapse of an n-dodecane molecule in H2O, CCl4, and a water-like Lennard-Jones solvent indicates t

125 investigated with a series of halomethanes (CCl4, CHCl3, CH2Cl2, and CH3Cl) using a FA-SIFT instrume

126 mmatory responses in a model of hepatotoxin (CCl4 )-induced hepatitis, but surprisingly exacerbated l

127 from d,l-butanediol, with hexafluoroacetone (CCl4, -40 degrees C) leads to the simultaneous formation

128 nces were observed between CTRL+CCl4 and HFD+CCl4 mice.

129 In CCl4 -cirrhotic rats, terutroban reduced liver fibrosis

130 In CCl4 dispersion forces dominate and planar complexes are

131 hotolysis (LFP, lambdaex = 355 nm) of 1-5 in CCl4 produces the corresponding aroylphenyl radicals (9-

132 n 1-chlorobenzimidazole and benzimidazole in CCl4/CH3OH/K2CO3 solution.

133 ng to a number of hydrogen bonding donors in CCl4, is described and is used to relate the observed sh

134 tissues, and levels increase dramatically in CCl4-treated rats, an animal model of oxidant injury.

135 The lifetimes of each in CCl4 have been found to be approximately 17-18 micros.

136 ation, and microthrombosis were evaluated in CCl4 and thioacetamide-cirrhotic rats treated with RVXB

137 and rapidly reversed fatal liver failure in CCl4-treated animals by restoring diseased hepatocytes r

138 ourfold increase of engrafted hepatocytes in CCl4-treated livers 10 days after transplantation which

139 es gfap, the inactivation marker of HSCs, in CCl4-treated liver.

140 lating LPS concentration did not increase in CCl4-treated mice.

141 ic macrophage and neutrophil infiltration in CCl4 -induced hepatitis and suppressed their phagocytic

142 The ALT level in CCl4 + VE-AF-L group was decreased to 38+/-16 units/mL,

143 lowered alanine transaminase (ALT) levels in CCl4-treated mice (196+/-79 vs. 2,107+/-235 U/mL; P < .0

144 se (eNOS) signaling pathway were measured in CCl4 and BDL cirrhotic rats treated with terutroban (30

145 AdoMet lowered the pathology in CCl4-treated mice as shown by transaminase levels, hemat

146 Dynamics of the free phenol in CCl4 or the mixed solvent are very similar, and dynamics

147 IR spectra of a series of phenols in CCl4 and 1% CD3CN/CCl4 provide relative acidities.

148 ot significantly change arterial pressure in CCl4 -cirrhotic rats but decreased it significantly in B

149 e P450 2E1, which plays an essential role in CCl4-induced necrotic injury, was not affected in p21-de

150 geminate recombination on two time scales in CCl4, approximately 50 and approximately 500 ps.

151 t of transplanted hepatocytes was similar in CCl4-treated and control livers, there was a fourfold in

152 an inactive heterodimer with it, whereas in CCl4-injured liver, the synthesis of gadd153/Chop10 is r

153 ue to decreased hepatic resistance, which in CCl4 -cirrhotic rats was linked to decreased hepatic fib

154 long-term liver injury, 7E and 51D inhibited CCl4 -induced cell damage, TGF-beta1 production, liver f

155 n two murine models of chronic liver injury (CCl4 and methionine-choline-deficient diet), Ccr6(-/-) m

156 ) controls were administered intraperitoneal CCl4 biweekly for up to 70 days, and the development of

157 g unit at baseline and 1 week after the last CCl4 treatment.

158 des ethanol, other substrates such as Me2SO, CCl4, isoniazid, and N,N-dimethylnitrosamine were cytoto

159 ed to WT mice in two separate murine models: CCl4 and bile duct ligation.

160 t detection of fibrosis in rat BDL and mouse CCl4 models of liver fibrosis.

161 In the presence of NADPH, CCl4 produced a concentration-dependent release of calci

162 tes a water nanodroplet from a bulk nonpolar CCl4 phase, ultrafast vibrational spectroscopy was used

163 the reaction of anisole with Cl2 in nonpolar CCl4 solution challenges two fundamental tenets of the t

164 rile for Pb as dispersive solvents, 60muL of CCl4 as extraction solvent for both analytes and 500muL

165 ty of CYP2E1, required for bio-activation of CCl4, nor AST and ALT activity in the plasma were affect

166 Administration of CCl4 also induced stronger hepatic injury in Jnk(Deltahe

167 ver fibrosis upon repeated administration of CCl4 Deficiency of IRF3 or STING prevented hepatocyte de

168 (MtnLacZ)] followed by the administration of CCl4.

169 mean of 24-fold following administration of CCl4.

170 d by bile duct ligation or administration of CCl4.

171 ed the isotopologue ions CCl3, CCl2, CCl (of CCl4) and CHCl3, CHCl2, CHCl (of CHCl3), respectively.

172 d day, administration of a nonlethal dose of CCl4 (2 mL/kg, intraperitoneally) yielded 70% mortality

173 dividual effects of a FFD or a micro dose of CCl4 in rats.

174 a challenge with a single necrogenic dose of CCl4, c-met conditional knockout mice exhibited impaired

175 cted intraperitoneally with a single dose of CCl4.

176 nistration of low, but hepatotoxic, doses of CCl4.

177 e gates rotate about their axis: the exit of CCl4 requires the activation energy of 12.7 kcal/mol (De

178 id not increase the direct hepatotoxicity of CCl4.

179 ALF model, 7-day survival after injection of CCl4 was 25%.

180 in a biphasic manner following injection of CCl4, with an early peak of p21 expression occurring in

181 L/6 (control) mice, were given injections of CCl4 (to induce fibrosis) or acetaminophen (to induce to

182 These mice were also given injections of CCl4, to increase liver fibrosis, for 8 weeks.

183 ice were given intraperitoneal injections of CCl4, twice weekly for 4 weeks.

184 in protecting the liver from toxic injury of CCl4 and preserving the hepatocyte ultrastructure.

185 xidation was not observed at these levels of CCl4, and the lag period for CCl4-induced release of cal

186 These results suggest that metabolism of CCl4 to reactive species by cytochrome P450 results in a

187 antial hepatic fibrosis requires 12 weeks of CCl4 administration.

188 However, following 6 weeks of CCl4 treatment, histochemical analyses showed markedly r

189 ice after 4 extra weeks (16 vs. 12 weeks) of CCl4 gavage.

190 uring a 28-day recovery period after 8 wk of CCl4 treatment, wild-type (WT) livers had significantly

191 s no beneficial effect of Nrf2 activation on CCl4 -induced liver injury and fibrosis.

192 as a function of their inhibitory effect on CCl4-induced lipid peroxidation of hepatic microsomes, e

193 jected to either bile duct ligation (BDL) or CCl4 treatment.

194 (+)-galactosamine and lipopolysaccharides or CCl4.

195 ed acetaminophen-, ethanol-, or ethanol plus CCl4 -induced liver injury.

196 han with the distribution of other potential CCl4 sources such as uncapped landfills or activities re

197 PARP inhibition not only prevented CCl4 -induced chronic liver inflammation and fibrosis, b

198 Antibody treatment prevented CCl4-mediated increases in early-immediate gene expressi

199 stellate cell (LSC) line derived from a rat CCl4-cirrhotic liver, we isolated 14 clones from a compl

200 ry induced by bile duct ligation or repeated CCl4 administration, including in animals with cirrhosis

201 In this setting, CCl4 is administered for 12 weeks after tail-vein inject

202 with acute fibrogenesis induced by a single CCl4 injection the half-life of I125-labeled pPB-HSA at

203 en nucleic acid bases in a nonpolar solvent (CCl4) are described.

204 oxyl stretch of phenol-OD in three solvents, CCl4, mesitylene (1, 3, 5 trimethylbenzene), and the mix

205 In in vivo antioxidant study, CCl4 induced oxidative stress on rats produced significa

206 AOT interfacial monolayer to the surrounding CCl4.

207 evated in mice with short-term and long-term CCl4 -induced liver injury.

208 Short-term CCl4 liver damage was earlier and more efficiently repai

209 d hepatitis induced by carbon tetrachloride (CCl4 ) and/or ethanol.

210 with cirrhosis due to carbon tetrachloride (CCl4 ) or bile duct ligation (BDL).

211 ethanol feeding and/or carbon tetrachloride (CCl4 ) treatment, and liver injury was assessed.

212 mouse model induced by carbon tetrachloride (CCl4 ), and a rat model induced by bile duct ligation (B

213 and chronic models of carbon tetrachloride (CCl4 )-induced liver injury and fibrosis, a model of bil

214 ver surgery as well as carbon tetrachloride (CCl4 )-mediated injury.

215 ficient mice following carbon tetrachloride (CCl4) administration.

216 ver regeneration after carbon tetrachloride (CCl4) administration.

217 r after treatment with carbon tetrachloride (CCl4) and into untreated controls.

218 ibrosis in response to carbon tetrachloride (CCl4) and that treatment of mice with an A2AR antagonist

219 nal-scale emissions of carbon tetrachloride (CCl4) are derived based on inverse modeling of atmospher

220 amage caused by either carbon tetrachloride (CCl4) exposure or by PHx.

221 ethylnitrosamine (DEN)/carbon tetrachloride (CCl4) extensively induced expression of DCLK1 (a CSC mar

222 ed to either saline or carbon tetrachloride (CCl4) for 6 wk.

223 e-weekly injections of carbon tetrachloride (CCl4) for 7 weeks.

224 J mice by injection of carbon tetrachloride (CCl4) or placement on a methionine-choline-deficient die

225 Mice were treated with carbon tetrachloride (CCl4) or with vehicle two times a week for 10 weeks and

226 r cirrhosis induced by carbon tetrachloride (CCl4) that recapitulates key features of human HCC.

227 ene were injected with carbon tetrachloride (CCl4) to induce fibrosis and coadministered either AdoMe

228 Carbon tetrachloride (CCl4) treatment induced IL-20 that further up-regulated

229 used three models: (i) carbon tetrachloride (CCl4) treatment, (ii) albumin-urokinase transgenic mouse

230 damage resulting from carbon tetrachloride (CCl4) treatment.

231 Carbon tetrachloride (CCl4) was fed by gavage to rats, and 2, 7, 14, and 28 da

232 s from rats exposed to carbon tetrachloride (CCl4), a potent fibrogenic stimulant.

233 of bromoform (CHBr3), carbon tetrachloride (CCl4), and dibromodichloromethane (CBr2Cl2) shows previo

234 stered intraperitoneal carbon tetrachloride (CCl4), and expression of IL-10 mRNA and protein in vivo

235 inofluorene (AAF) with carbon tetrachloride (CCl4), indicating a conserved response to chronic liver

236 partial hepatectomy or carbon tetrachloride (CCl4)-induced acute injury.

237 We investigated carbon tetrachloride (CCl4)-induced fibrosis and LPS-induced acute liver injur

238 in C57Bl/6J mice with carbon tetrachloride (CCl4)-induced fibrosis.

239 e to acetaminophen- or carbon tetrachloride (CCl4)-induced liver damage; the level of activation corr

240 6 mice with or without carbon tetrachloride (CCl4)-induced liver fibrosis.

241 in an in vivo model of carbon tetrachloride (CCl4)-induced liver fibrosis.

242 miR-378d) declines in carbon tetrachloride (CCl4)-treated compared with corn-oil-treated mice.

243 taminophen (APAP)- and carbon tetrachloride (CCl4)-treated mice.

244 eritoneal injection of carbon tetrachloride (CCl4).

245 iver injury induced by carbon tetrachloride (CCl4).

246 oliferation induced by carbon tetrachloride (CCl4).

247 chemical hepatotoxin, carbon tetrachloride (CCl4).

248 ritoneal injections of carbon tetrachloride (CCl4).

249 he liver's response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the n

250 ice exposed to chronic carbon tetrachloride (CCl4); receptor density was derived from published liter

251 at diet) and fibrotic (carbon tetrachloride [CCl4]) challenge.

252 centrilobular regions (carbon tetrachloride [CCl4]) or periportal regions (allyl alcohol [AA]).

253 rine isotope analysis of tetrachloromethane (CCl4) and trichloromethane (CHCl3) was explored by both,

254 nd the requirement for NADPH, indicates that CCl4 metabolism is required for the activation of calciu

255 In view of that, CCl4 (but also (CH3)3CBr) was proposed to escape from, a

256 The CCl4-induced calcium release was blocked by ruthenium re

257 tion, there is only complexed phenol; in the CCl4 solution, there is only uncomplexed phenol; and in

258 ble source of mesenchymal stem cells, in the CCl4-induced acute liver injury model.

259 n sham-treated rats (5.7 +/- 4.2) and in the CCl4-treated mice (18.3 +/- 6.5) compared with baseline

260 te computational spectral intensities of the CCl4-H2O and DCE-H2O interfaces that are directly compar

261 Inhibition of the CCl4-induced release of calcium by 4-methylpyrazole and

262 ping experiments with PBN; PBN prevented the CCl4-induced calcium release, presumably by interacting

263 ol or cysteamine could partially reverse the CCl4-induced calcium release, whereas GSH was ineffectiv

264 p within 1.8 picoseconds and then out to the CCl4 within 10 picoseconds.

265 - to 40-picosecond transfer of energy to the CCl4.

266 2 per thousand (CHCl3) and 0.4 per thousand (CCl4), which are only about twice as large as 0.1 per th

267 d an increased catalase activity compared to CCl4-treated mice.

268 early response in stellate cells exposed to CCl4, coinciding with increased M6P/IGFIIR transcript le

269 or 5 weeks and superimposed with exposure to CCl4, we tested the hypothesis that moderate ethanol con

270 exacerbated liver fibrosis upon exposure to CCl4.

271 xacerbates hepatic fibrosis upon exposure to CCl4.

272 hanol-fed ALDH2(-/-) mice were more prone to CCl4 -induced liver inflammation and fibrosis than ethan

273 Small cholangiocytes appear resistant to CCl4-induced apoptosis, and proliferate and transiently

274 gly, p21-deficient animals were resistant to CCl4-induced necrotic injury, indicating that rapid indu

275 that livers of dnp300 mice are resistant to CCl4-mediated injury and have reduced apoptosis but have

276 We have examined liver response to CCl4 treatments using old WT mice and young C/EBPalpha-S

277 one- to two-thirds of the US national total CCl4 emission during 2008-2012.

278 ression phase of two murine models of toxic (CCl4 ) and metabolic (methionine-choline-deficient diet)

279 the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other han

280 the normal liver and greatly increases upon CCl4 treatment.

281 reviously, ATF3 is induced in the liver upon CCl4 treatment.

282 ional C57BL/6 mice were made cirrhotic using CCl4 gavage.

283 he interfaces of carbon tetrachloride-water (CCl4-H2O) and 1,2-dichloroethane-water (DCE-H2O).

284 m simulation of the same peptides in a water/CCl4 biphasic cell were compared with the results of the

285 simulation was either parallel to the water/CCl4 interface or in a perpendicular/insertion mode.

286 e peptide properly with respect to the water/CCl4 interface.

287 ar dynamics (MD) simulation in a TIP3P water/CCl4 biphasic solvent system as a mimic for the water-me

288 required for the 1A/B interconversion, when CCl4 occupies the cavity of 1.

289 readily alpha-halogenated in KOH-t-BuOH with CCl4 or CBrCl3.

290 liver fibrosis, WT mice were challenged with CCl4 for 4-6 weeks.

291 Rats were fed alcohol or injected with CCl4 to cause alcohol-induced liver injury and an early

292 we performed chronic treatments of mice with CCl4.

293 The low blood pressure of rats with CCl4-induced cirrhosis was similarly reversed by SR14171

294 ields for the radical trapping reaction with CCl4 as a function of solvent viscosity.

295 -overexpressing transgenic mice treated with CCl4 were susceptible to the development hepatic fibrosi

296 uced in fibrotic livers of rats treated with CCl4.

297 After 70 days of treatment with CCl4, IL-10-/- mice showed significantly more severe fib

298 d over 100-fold 6 hours after treatment with CCl4, reaching a peak of 140-fold above baseline by 10 h

299 liver DNA of F344 rats after treatment with CCl4, suggesting that tissue lipid peroxidation is a lik

300 r isolated, perfused livers with and without CCl4 intoxication and (2) a set of in vivo experiments.