ライフサイエンスコーパス: carbon tetrachloride

1 ter administration of diethylnitrosamine and carbon tetrachloride.

2 in female mice by chronic administration of carbon tetrachloride.

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

4 t also ameliorated liver fibrosis induced by carbon tetrachloride.

5 intraperitoneal injection of the hepatotoxin carbon tetrachloride.

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

7 duced by partial hepatectomy and exposure to 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 thoxycarbonyl-1,4-dihydrocollidine (DDC) and carbon tetrachloride.

14 ated catalytic activity for the reduction of carbon tetrachloride.

15 hydrolysis of the environmental contaminant carbon tetrachloride.

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

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

18 Carbon tetrachloride administration caused an intense de

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

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

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

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

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

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

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

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

27 Carbon tetrachloride and cell transplantation produced h

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

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

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

31 Carbon tetrachloride and methionine/choline deficiency w

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 5A/B-null mice (STAT5-LKO) were treated with carbon tetrachloride (CCl(4)), and histological analyses

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

98 1/Cip1, and p27Kip1-deficient mice following carbon tetrachloride (CCl4) administration.

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

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

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

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

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

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

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

106 20 g) mice using thrice-weekly injections of carbon tetrachloride (CCl4) for 7 weeks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

126 -378a-3p, miR-378b and miR-378d) declines in carbon tetrachloride (CCl4)-treated compared with corn-o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 Rats with carbon tetrachloride-induced cirrhosis and ascites were

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

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

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

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

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

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

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

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

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

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

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

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

176 Cirrhosis was induced by carbon tetrachloride inhalation.

177 Upon carbon tetrachloride injection or bile duct ligation sur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

192 Carbon tetrachloride liver injury was used to demonstrat

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

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

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

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

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

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

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

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

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

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

203 95% confidence interval (CI): 1.1, 1.8) and carbon tetrachloride (OR = 2.3, 95% CI: 1.3, 4.0).

204 , 95% confidence interval (CI): 1.06, 2.69), carbon tetrachloride (OR = 2.33, 95% CI: 1.23, 4.40), an

205 , 95% CI: 2.03, 9.62; P(interaction) < 0.01; carbon tetrachloride: OR = 5.08, 95% CI: 1.82, 14.15; P(

206 Treatment with DDC and carbon tetrachloride significantly facilitated the adeno

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

225 artial hepatectomy before transplantation or carbon tetrachloride treatment following transplantation

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

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

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

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

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

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

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

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

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

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

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

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