ライフサイエンスコーパス: carbon tetrachloride

1 hydrolysis of the environmental contaminant carbon tetrachloride.

2 the combination of chloroform, benzene, and carbon tetrachloride.

3 in female mice by chronic administration of carbon tetrachloride.

4 llidine (DDC) diet or by injecting them with carbon tetrachloride.

5 t also ameliorated liver fibrosis induced by carbon tetrachloride.

6 intraperitoneal injection of the hepatotoxin carbon tetrachloride.

7 olyphenol in green tea, in mice treated with carbon tetrachloride.

8 cirrhosis was induced with phenobarbital and carbon tetrachloride.

9 rried out for dialanine peptide in water and carbon tetrachloride.

10 otic septae in livers from rats treated with carbon tetrachloride.

11 9, 10-diphenylanthracene (DPA) dissolved in carbon tetrachloride.

12 ous areas by targeted hepatic ablations with carbon tetrachloride.

13 fat, high-cholesterol, high-fructose diet or carbon tetrachloride.

14 er fibrosis induced by bile duct ligation or carbon tetrachloride.

15 ter administration of diethylnitrosamine and carbon tetrachloride.

16 duced by partial hepatectomy and exposure to carbon tetrachloride.

17 hylbenzene, hexane, pentane, chloroform, and carbon tetrachloride.

18 thoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride.

19 ated catalytic activity for the reduction of carbon tetrachloride.

20 larly, carbon tetrabromide (296% [245-346]), carbon tetrachloride (180% [163-196]), and 1,1,1,3,3,3-h

21 binding enthalpy of 4-fluorophenol to 1a in carbon tetrachloride (-23.5 +/- 0.3 kJ mol(-1)) interloc

22 Carbon tetrachloride administration caused an intense de

23 ine liver injury was induced by twice-weekly carbon tetrachloride administration for 8 weeks.

24 irradiated NOD/SCID/MPSVII mice followed by carbon tetrachloride administration to induced liver dam

25 In response to carbon tetrachloride administration, when wild-type hepa

26 s from these mice had reduced fibrosis after carbon tetrachloride administration.

27 In response to chronic treatment with carbon tetrachloride, all experimental mice, but none of

28 dels of liver injury (bile duct ligation and carbon tetrachloride) also exhibited elevated PGE2, redu

29 wo fibrosis-associated HCC models induced by carbon tetrachloride and a high-fat, high-carbohydrate d

30 ing animal models of hepatoxicity induced by carbon tetrachloride and acetaminophen, we found that bo

31 In vivo, SEMA7A KO mice treated with carbon tetrachloride and bile duct ligation developed re

32 genic/wound-healing response to both chronic carbon tetrachloride and bile duct ligation induced inju

33 Carbon tetrachloride and cell transplantation produced h

34 conventional mice were made cirrhotic using carbon tetrachloride and compared with controls in GF an

35 are the cell of origin of HCA and HCC in DEN/carbon tetrachloride and DEN/TCPOBOP induced liver tumor

36 e and after a single dose of the hepatotoxin carbon tetrachloride and hybridized them against high-de

37 In the carbon tetrachloride and methionine-choline-deficient di

38 Carbon tetrachloride and methionine/choline deficiency w

39 tes in the VUV spectral region at 9.33 eV of carbon tetrachloride and strong vibronic coupling result

40 In this case, the mobile phase was carbon tetrachloride and the stationary phase was a C18

41 nol, methanol, N-methyl-2-pyrrolidone (NMP), carbon tetrachloride and water) confined to 2D graphene

42 ile duct ligation [BDL] or administration of carbon tetrachloride), and CPEB4-knockout mice.

43 sis was induced in rats by administration of carbon tetrachloride, and activation was monitored as th

44 the livers of rats exposed to acetaminophen, carbon tetrachloride, and allyl alcohol, respectively.

45 hexafluoride, methyl ethyl ketone, acetone, carbon tetrachloride, and ammonia.

46 n volatile organic solvents such as benzene, carbon tetrachloride, and hexane.

47 ed emissions of several chlorofluorocarbons, carbon tetrachloride, and hydrofluorocarbons, are underm

48 re- mice) were treated with a single dose of carbon tetrachloride, and liver injury and repair were a

49 s induced in these mice by administration of carbon tetrachloride, and liver tissues and HSCs were co

50 , n-dodecane, n-undecyl alcohol, chloroform, carbon tetrachloride, and water.

51 n contrast to models of cirrhosis induced by carbon tetrachloride, aquaporin-2 expression in CBDL-ind

52 DLLME was performed using carbon tetrachloride as extractive solvent and acetonitr

53 including trichloroethylene, vinyl chloride, carbon tetrachloride, benzene, and chloroform, are commo

54 show colocalization of PDGFRalpha in murine carbon tetrachloride, bile duct ligation, and 0.1% 3,5-d

55 ry from acute toxic liver injuries (APAP and carbon tetrachloride) by increasing tumour necrosis fact

56 d insecticide dieldrin, the fumigant mixture carbon-tetrachloride/carbon disulfide, and the fungicide

57 c stellate cells following liver injury from carbon tetrachloride (CCl 4 ) or thioacetamide (TAA).

58 ile duct ligation (BDL) (2, 4, and 8 weeks), carbon tetrachloride (CCl(4) ) (3 weeks), and 3,5-dietho

59 ted to chronic experimental injury models of carbon tetrachloride (CCl(4) ) administration and surgic

60 uced by either intraperitoneal injections of carbon tetrachloride (CCl(4) ) for up to 12 weeks (rat a

61 NOX2 knockout (NOX2KO) mice by way of either carbon tetrachloride (CCl(4) ) injection or bile duct li

62 and exposure to perchloroethylene (PERC) and carbon tetrachloride (CCl(4) ) tended toward significanc

63 bridization that Wnts are activated by acute carbon tetrachloride (CCl(4) ) toxicity.

64 groups of BDL and cirrhotic rats induced by carbon tetrachloride (CCl(4) ) were treated for 5 days w

65 Similarly, Rac mice treated with carbon tetrachloride (CCl(4)) accumulated greater number

66 either bile duct ligation (BDL) or repeated carbon tetrachloride (CCl(4)) administration.

67 ury and fibrosis produced in mice by chronic carbon tetrachloride (CCl(4)) administration.

68 in relation to fibrosis produced by chronic carbon tetrachloride (CCl(4)) administration.

69 In this study, carbon tetrachloride (CCl(4)) and 1-(2-pyridylazo)2-naph

70 irrhosis was induced using phenobarbital and carbon tetrachloride (CCL(4)) and animals were studied o

71 Furthermore, we find that in this region, carbon tetrachloride (CCl(4)) and dichlorodifluoromethan

72 on and angiogenesis with mice challenged for Carbon tetrachloride (CCl(4)) and dimethylnitrosamine (D

73 ation and hepatic fibrosis resolution in the carbon tetrachloride (CCl(4)) and fructose, palmitate, c

74 ollowing a chronic liver injury, we injected carbon tetrachloride (CCl(4)) biweekly into mice lacking

75 er fibrosis was induced by administration of carbon tetrachloride (CCl(4)) for 2 weeks.

76 Exacerbated carbon tetrachloride (CCl(4)) hepatoxicity was also obse

77 response upon exposure to the hepatotoxicant carbon tetrachloride (CCl(4)) in male rats.

78 tion may attenuate liver necrosis induced by carbon tetrachloride (CCl(4)) in myeloid-specific signal

79 er against injury and fibrogenesis caused by carbon tetrachloride (CCl(4)) in rats and further explor

80 impact of both acute and chronic exposure to carbon tetrachloride (CCl(4)) in the livers of FGF1- and

81 Here, we demonstrated that carbon tetrachloride (CCl(4)) injection into mice activa

82 atically ameliorates liver injury induced by carbon tetrachloride (CCl(4)) injections.

83 We induced liver fibrosis by repetitive carbon tetrachloride (CCl(4)) injections.

84 Carbon tetrachloride (CCl(4)) interferes with triglyceri

85 Using carbon tetrachloride (CCl(4)) intoxication as a model of

86 Carbon tetrachloride (CCl(4)) intoxification in rodents

87 Klf6 isoforms decreased in response to acute carbon tetrachloride (CCl(4)) liver injury and culture-i

88 In this study, we used carbon tetrachloride (CCl(4)) liver injury to induce a d

89 In the carbon tetrachloride (CCl(4)) model of liver fibrosis, q

90 ibrosis was induced in BALB/c mice by either carbon tetrachloride (CCl(4)) or bile duct ligation (BDL

91 roduced Cl(2) is extracted and stored in the carbon tetrachloride (CCl(4)) or mineral spirit flow.

92 Mouse hepatofibrosis was induced by carbon tetrachloride (CCl(4)) or thioacetamide.

93 Mice were then given diethylnitrosamine and carbon tetrachloride (CCl(4)) to induce mutations, chron

94 regulated after bile duct ligation (BDL) and carbon tetrachloride (CCl(4)) treatment in hepatocytes,

95 Previous studies showed that following acute carbon tetrachloride (CCl(4)) treatment, interleukin-6 n

96 Following acute carbon tetrachloride (CCl(4)) treatment, we found that I

97 ng bile duct ligation for 21 days or chronic carbon tetrachloride (CCl(4)) treatment.

98 One month after transplantation, carbon tetrachloride (CCl(4)) was administered into the

99 thoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride (CCl(4)) were employed to induce ch

100 5A/B-null mice (STAT5-LKO) were treated with carbon tetrachloride (CCl(4)), and histological analyses

101 entrolobular injury, such as that induced by carbon tetrachloride (CCl(4)), and to dimethylnitrosamin

102 atectomy, acute or chronic administration of carbon tetrachloride (CCl(4)), choline-deficient diet su

103 Rats were treated with carbon tetrachloride (CCl(4)), or olive oil control, for

104 t not female mice from thioacetamide (TAA)-, carbon tetrachloride (CCl(4))-, or bile duct ligation (B

105 iNKT-deficient mice are more susceptible to carbon tetrachloride (CCl(4))-induced acute liver injury

106 cyte proliferation during regeneration after carbon tetrachloride (CCl(4))-induced injury.

107 We therefore investigated neoangiogenesis in carbon tetrachloride (CCl(4))-induced liver fibrosis in

108 N)-induced liver tumor model and the chronic carbon tetrachloride (CCl(4))-induced liver fibrosis mod

109 e role of the CX3CL1-CX3CR1 interaction in a carbon tetrachloride (CCl(4))-induced liver inflammation

110 f human cirrhotic liver, a Western diet- and carbon tetrachloride (CCl(4))-induced minipig NASH model

111 Theaceae) were investigated with a study of carbon tetrachloride (CCl(4))-induced oxidative stress a

112 egeneration following partial hepatectomy or carbon tetrachloride (CCl(4))-mediated liver injury and

113 nsfer may induce reductive dechlorination of carbon tetrachloride (CCl(4)).

114 ing 12 weeks of intraperitoneal injection of carbon tetrachloride (CCl(4)).

115 type and egr-1(-/-) mice to acute or chronic carbon tetrachloride (CCl(4)).

116 e injuries induced by HPA or hepatoxic agent carbon tetrachloride (CCl(4)).

117 maturation and after acute injury induced by carbon tetrachloride (CCl(4)).

118 paracetamol (APAP; 3.5 and 1.0 mmol/kg), or carbon tetrachloride (CCl(4); 1.0 and 0.2 mmol/kg).

119 in experimental mouse models of hepatotoxic (carbon tetrachloride [CCl(4)] intoxication) and cholesta

120 nd hepatotoxin-mediated hepatitis induced by carbon tetrachloride (CCl4 ) and/or ethanol.

121 ortal pressure in rats with cirrhosis due to carbon tetrachloride (CCl4 ) or bile duct ligation (BDL)

122 ice were subjected to ethanol feeding and/or carbon tetrachloride (CCl4 ) treatment, and liver injury

123 lnitrosamine (DEN), a mouse model induced by carbon tetrachloride (CCl4 ), and a rat model induced by

124 d fibrosis using acute and chronic models of carbon tetrachloride (CCl4 )-induced liver injury and fi

125 tion in response to liver surgery as well as carbon tetrachloride (CCl4 )-mediated injury.

126 1/Cip1, and p27Kip1-deficient mice following carbon tetrachloride (CCl4) administration.

127 process, we studied liver regeneration after carbon tetrachloride (CCl4) administration.

128 enhanced in 2 models of acute liver injury: carbon tetrachloride (CCl4) and acetaminophen.

129 nically into mice 24 hr after treatment with carbon tetrachloride (CCl4) and into untreated controls.

130 onsumption increases fibrosis in response to carbon tetrachloride (CCl4) and that treatment of mice w

131 National-scale emissions of carbon tetrachloride (CCl4) are derived based on inverse

132 th selective hepatic damage caused by either carbon tetrachloride (CCl4) exposure or by PHx.

133 Diethylnitrosamine (DEN)/carbon tetrachloride (CCl4) extensively induced expressi

134 littermates were exposed to either saline or carbon tetrachloride (CCl4) for 6 wk.

135 20 g) mice using thrice-weekly injections of carbon tetrachloride (CCl4) for 7 weeks.

136 ury was induced in BoyJ mice by injection of carbon tetrachloride (CCl4) or placement on a methionine

137 Mice were treated with carbon tetrachloride (CCl4) or with vehicle two times a

138 mpetent mice with liver cirrhosis induced by carbon tetrachloride (CCl4) that recapitulates key featu

139 he beta-gal reporter gene were injected with carbon tetrachloride (CCl4) to induce fibrosis and coadm

140 Carbon tetrachloride (CCl4) treatment induced IL-20 that

141 We used three models: (i) carbon tetrachloride (CCl4) treatment, (ii) albumin-urok

142 partial hepatectomy or damage resulting from carbon tetrachloride (CCl4) treatment.

143 Carbon tetrachloride (CCl4) was fed by gavage to rats, a

144 eased in stellate cells from rats exposed to carbon tetrachloride (CCl4), a potent fibrogenic stimula

145 mulated 2D TTR spectra of bromoform (CHBr3), carbon tetrachloride (CCl4), and dibromodichloromethane

146 Rats were administered intraperitoneal carbon tetrachloride (CCl4), and expression of IL-10 mRN

147 ury was induced by chronic administration of carbon tetrachloride (CCl4), and rifaximin was administe

148 induced by 2-acetylaminofluorene (AAF) with carbon tetrachloride (CCl4), indicating a conserved resp

149 cl-5 after two-thirds partial hepatectomy or carbon tetrachloride (CCl4)-induced acute injury.

150 the TNF-alpha inhibitor etanercept inhibits carbon tetrachloride (CCL4)-induced fibrogenesis in an E

151 We investigated carbon tetrachloride (CCl4)-induced fibrosis and LPS-ind

152 or vehicle as control) in C57Bl/6J mice with carbon tetrachloride (CCl4)-induced fibrosis.

153 phorylation in response to acetaminophen- or carbon tetrachloride (CCl4)-induced liver damage; the le

154 l (HSC) proliferation in an in vivo model of carbon tetrachloride (CCl4)-induced liver fibrosis.

155 as performed in C57Bl/6 mice with or without carbon tetrachloride (CCl4)-induced liver fibrosis.

156 -378a-3p, miR-378b and miR-378d) declines in carbon tetrachloride (CCl4)-treated compared with corn-o

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

158 gle near-lethal intraperitoneal injection of carbon tetrachloride (CCl4).

159 urred normally after liver injury induced by carbon tetrachloride (CCl4).

160 jury and hepatocyte proliferation induced by carbon tetrachloride (CCl4).

161 lowing exposure to the chemical hepatotoxin, carbon tetrachloride (CCl4).

162 or by repeated intraperitoneal injections of carbon tetrachloride (CCl4).

163 pping manners during the liver's response to carbon tetrachloride (CCl4): the level of gadd153/Chop10

164 the hepatic ECM from mice exposed to chronic carbon tetrachloride (CCl4); receptor density was derive

165 fter metabolic (high-fat diet) and fibrotic (carbon tetrachloride [CCl4]) challenge.

166 h selective damage of centrilobular regions (carbon tetrachloride [CCl4]) or periportal regions (ally

167 n of KCa3.1 aggravated liver fibrosis during carbon tetrachloride challenge but did not change hemody

168 In the presence of carbon tetrachloride, chloride 7 is formed in addition t

169 rganic pollutants, including vinyl chloride, carbon tetrachloride, chloroform and benzene.

170 llutants, including TCE, ethylene dibromide, carbon tetrachloride, chloroform, and vinyl chloride.

171 oluene, o-xylene, cymene, tert-butylbenzene, carbon tetrachloride, chloroform, chlorobenzene, tetrach

172 and fibrosis after BDL or administration of carbon tetrachloride compared with wild-type mice.

173 ducts formed during reaction between FeS and carbon tetrachloride (CT) at pH 7 and 8.

174 The reductive dechlorination of carbon tetrachloride (CT) by Fe(II)-Fe(III) hydroxide (g

175 In this study, carbon tetrachloride (CT) dehalogenation by the chloride

176 henobarbital (PB), lipopolysaccharide (LPS), carbon tetrachloride (CT), thioacetamide (THA), and cypr

177 degradation of chlorinated alkanes, such as carbon tetrachloride (CT); 1,1,1-trichloroethane (1,1,1-

178 nflammatory genes was reduced in livers from carbon tetrachloride-exposed PHD1(-/-) mice.

179 ID mice and rats underwent liver injury with carbon tetrachloride exposure or partial hepatectomy.

180 inase plasminogen activator transgenic mice, carbon tetrachloride exposure, and diethylnistrosamine t

181 contrast, the non-hepatocarcinogenic agent, carbon tetrachloride, failed to induce p53, and caused a

182 Liver injury was induced with carbon tetrachloride, fibrosis was quantitated, and Th1/

183 blished in rat livers by chronic injury with carbon tetrachloride followed by recovery with or withou

184 In contrast, rats treated with carbon tetrachloride for 1 or 3 mo showed 84% +/- 5% and

185 ned directly in animals, where withdrawal of carbon tetrachloride for 2 wk after significant liver in

186 was induced in BALB/c mice by administering carbon tetrachloride for 4 or 8 weeks.

187 c liver disease was induced by administering carbon tetrachloride for 8 weeks.

188 o-tert-butyl alcohol, tetramethylsilane, and carbon tetrachloride have been carried out.

189 After carbon tetrachloride, HIF-1alpha was activated in HSCs.

190 Liver injury was induced in vivo by carbon tetrachloride i.p. injection or bile duct ligatio

191 Liver fibrosis was induced utilizing carbon tetrachloride in wild-type (WT) and PHD1(-/-) mic

192 otein (mGFP) Cre-reporter after injection of carbon tetrachloride, in liver and isolated HSCs, and a

193 ition of KCa3.1 was evaluated in mice during carbon tetrachloride induced hepatic fibrogenesis.

194 ction on portal pressure in rat livers after carbon tetrachloride induced injury (including cirrhosis

195 In acetaminophen (APAP)- or carbon tetrachloride-induced acute liver injuries, NR2E3

196 and vascular tissue obtained from rats with carbon tetrachloride-induced cirrhosis and ascites (n =

197 Rats with carbon tetrachloride-induced cirrhosis and ascites were

198 Sixteen control rats and 16 rats with carbon tetrachloride-induced cirrhosis were studied.

199 In carbon tetrachloride-induced fibrosis and zymosan-induce

200 ve, but can reverse the fibrotic response in carbon tetrachloride-induced fibrosis in mouse models.

201 The junD-/- mice were protected from carbon tetrachloride-induced fibrosis.

202 ce fed the HFD, nor did it protect mice from carbon tetrachloride-induced fibrosis.

203 Such depletion protected mice from carbon tetrachloride-induced hepatic fibrosis, whereas g

204 iated liver protection was confirmed using a carbon tetrachloride-induced liver fibrosis model in wil

205 in disease, we used (99m)Tc-mebrofenin in a carbon tetrachloride-induced liver injury model in Fisch

206 nA) but are less extensively elevated in the carbon tetrachloride-induced liver injury model.

207 pair after either 70% partial hepatectomy or carbon tetrachloride-induced liver injury.

208 protein expression is elevated in mice with carbon tetrachloride-induced liver injury.

209 liver fibrosis using T(1)-weighted MRI in a carbon tetrachloride-induced mouse liver injury model.

210 In a carbon tetrachloride-induced mouse model of hepatic fibr

211 Monocrotaline sensitized the liver to carbon tetrachloride-induced necrosis, which advanced tr

212 rahepatic injection in normal and cirrhotic (carbon tetrachloride-induced) mice.

213 Cirrhosis was generated by carbon tetrachloride inhalation in wild-type (WT) and No

214 formed in cirrhotic rats (induced by chronic carbon tetrachloride inhalation) and weight-matched norm

215 Cirrhosis was induced by carbon tetrachloride inhalation.

216 Upon carbon tetrachloride injection or bile duct ligation sur

217 c injury inflicted by iterative hepatotoxin (carbon tetrachloride) injection and bile duct ligation,

218 ver fibrosis was created in rats by means of carbon tetrachloride injections over an 8-week period.

219 oisoning and reduced fibrosis after repeated carbon tetrachloride injections.

220 haracterized these cells in normal liver, in carbon tetrachloride-injured liver, and in several model

221 sion observed in the partial-hepatectomy and carbon tetrachloride injury models, we found no differen

222 After acute acetaminophen or carbon tetrachloride injury no contribution of HNF1beta(

223 During hepatic injury due to either carbon tetrachloride injury or bile duct ligation, we de

224 we examined Foxf1 +/- liver repair following carbon tetrachloride injury, a known model for stellate

225 albeit transient reduction in fibrosis after carbon tetrachloride injury, associated with increased H

226 Thy-1(+) cells proliferate moderately after carbon tetrachloride injury, in all models of OC-mediate

227 ular injury in knockout mice despite ongoing carbon tetrachloride insult, associated with increased n

228 e liver was observed after administration of carbon tetrachloride into SPlucTg mice.

229 n were investigated in bile duct-ligated and carbon tetrachloride intoxicated rats.

230 or moderate ethanol ingestion combined with carbon tetrachloride intoxication (ethanol/CCl(4) ).

231 er (16%) or Western diet in combination with carbon tetrachloride intoxication for 7 weeks to induce

232 inhibit liver fibrogenesis induced by either carbon tetrachloride intoxication or bile duct ligation

233 cts of RLN were studied after 8 and 16 weeks carbon tetrachloride intoxication, following bile duct l

234 Liver fibrosis induced by carbon tetrachloride is attenuated by thyroid hormone ad

235 atocyte DNA synthesis, and in mice receiving carbon tetrachloride, it reduced fibrosis.

236 Carbon tetrachloride liver injury was used to demonstrat

237 Following 12 weeks of Western diet/carbon tetrachloride, MASH fibrosis was identified in C5

238 icity in cultured cells as well as increased carbon tetrachloride-mediated liver damage in a mouse mo

239 ice expressing human RXFP1 gene treated with carbon tetrachloride, ML290 significantly reduced collag

240 Effects of rapamycin were investigated in a carbon tetrachloride model of hepatic fibrosis in rats a

241 ns are recapitulated in the well-established carbon tetrachloride model of liver fibrosis in which Ep

242 tic regulatory protein EZH2 were used in the carbon tetrachloride model of liver fibrosis.

243 In the carbon tetrachloride mouse model of fibrosis, pharmacolo

244 t animal models (bile duct ligation: n = 31, carbon tetrachloride: n = 12, thioacetamide: n = 12, cho

245 After liver injury by toxins such as carbon tetrachloride or after surgical resection, partia

246 same irradiation conditions in air-saturated carbon tetrachloride or deuterated chloroform produced a

247 nsisting of mostly nonpolar solvents such as carbon tetrachloride or ethyl acetate/hexane and 2-5% of

248 f two hepatocyte-like cell lines with either carbon tetrachloride or heat shock induced Gdf15 mRNA ex

249 ealthy Fischer 344 rats or rats treated with carbon tetrachloride or intrasplenic cell transplantatio

250 After either pericentral injury with carbon tetrachloride or periportal injury with 3,5-dieth

251 Advanced liver fibrosis was induced by carbon tetrachloride or thioacetamide in TG2(-/-) mice a

252 tly decreased, but chronic administration of carbon tetrachloride or thioacetamide led to a comparabl

253 95% confidence interval (CI): 1.1, 1.8) and carbon tetrachloride (OR = 2.3, 95% CI: 1.3, 4.0).

254 , 95% confidence interval (CI): 1.06, 2.69), carbon tetrachloride (OR = 2.33, 95% CI: 1.23, 4.40), an

255 in 12 livers from mice treated with vehicle, carbon tetrachloride, or diethylnitrosamine.

256 , 95% CI: 2.03, 9.62; P(interaction) < 0.01; carbon tetrachloride: OR = 5.08, 95% CI: 1.82, 14.15; P(

257 urce to prepare high-lying Rydberg states of carbon tetrachloride, our measurements reveal the local

258 Treatment with DDC and carbon tetrachloride significantly facilitated the adeno

259 nyl bisimide cyclophane in methylcyclohexane/carbon tetrachloride solutions with a quantum yield (QY)

260 phenol complexation to benzene in a benzene-carbon tetrachloride solvent mixture were measured in re

261 bers relative to its noninteracting value in carbon tetrachloride solvent.

262 ine, we introduced further liver injury with carbon tetrachloride subsequent to cell transplantation.

263 ter administration of diethylnitrosamine and carbon tetrachloride than control mice.

264 tissue remodeling and regeneration, we used carbon tetrachloride to induce an acute liver injury in

265 ne (DEN), followed by multiple injections of carbon tetrachloride to induce carcinogenesis and fibros

266 itrosamine (DEN) followed by weekly doses of carbon tetrachloride to induce liver fibrosis and tumori

267 e to induce cholestatic injury or were given carbon tetrachloride to induce liver fibrosis.

268 ay a role in liver fibrosis regression using carbon tetrachloride to induce liver injury.

269 proliferation in vivo, mice were exposed to carbon tetrachloride to induce liver regeneration follow

270 creased 35-fold after treatment of rats with carbon tetrachloride to induce oxidant stress.

271 o conventional organic solvents ranging from carbon tetrachloride to methanol.

272 repeated administration of thioacetamide or carbon tetrachloride to mice; mice were then exposed to

273 rried out in both solvent systems with added carbon tetrachloride to study how Lewis acid affected th

274 were activated in hepatocytes in response to carbon tetrachloride toxic injury.

275 We evaluated liver regeneration after carbon tetrachloride toxic liver injury in mice with con

276 cant reduction of liver fibrosis compared to carbon tetrachloride-treated littermate mice.

277 model of liver fibrosis in which EphB2(-/-) carbon tetrachloride-treated mice showed a significant r

278 ined the effects of green tea polyphenols in carbon tetrachloride-treated mice, a model of liver inju

279 al variables of liver injury observed in the carbon tetrachloride-treated mice.

280 Fibrosis is completely attenuated in carbon tetrachloride-treated, B cell-deficient microMT m

281 ivated in the regenerating liver following a carbon tetrachloride treatment and that the level of Gpc

282 artial hepatectomy before transplantation or carbon tetrachloride treatment following transplantation

283 unocompromised murine hosts with and without carbon tetrachloride treatment to assess the effects of

284 liver regeneration (partial hepatectomy and carbon tetrachloride treatment), and that this response

285 re subjected to chronic liver injury through carbon tetrachloride treatment, bile duct ligation, and

286 ull mice were more resistant to damage after carbon tetrachloride treatment.

287 in livers and isolated HSCs 30-45 days after carbon tetrachloride was no longer administered, despite

288 ch clear necrotic cells from the liver after carbon tetrachloride, was not affected by HIF-1alpha del

289 ent liquid-liquid systems: the interfaces of carbon tetrachloride-water (CCl4-H2O) and 1,2-dichloroet

290 Mice with liver cirrhosis induced by carbon tetrachloride were injected with 1 x 10(5) non-tr

291 of acute and chronic liver injury induced by carbon tetrachloride were studied in LEA rats.

292 correct 4 weeks after the discontinuation of carbon tetrachloride were subjected to intrasplenic rat

293 hloronitrobenzene, 2-chloroacetophenone, and carbon tetrachloride) were used as kinetic CRPs.

294 on is most strong in the least polar-solvent carbon tetrachloride where the ethanol-cholesterol equil

295 nduced by a combination of high-fat diet and carbon tetrachloride, where hepatic cells become senesce

296 Data have been collected primarily in carbon tetrachloride, where Oct(3)N(+)-H...A(-) contact