ライフサイエンスコーパス: CCL4

1 ritoneal injections of carbon tetrachloride (CCl4).

2 F2, IL6, and chemokine (C-C motif) ligand 4 (CCL4).

3 ne-related protein tyrosine kinase activity (CCL4).

4 tection Agency's candidate contaminant list (CCL4).

5 1, CXCL7 and CXCL8 and lower blood levels of CCL4.

6 iding hazardous chlorinated solvents such as CCl4.

7 we performed chronic treatments of mice with CCl4.

8 (+)-galactosamine and lipopolysaccharides or CCl4.

9 exacerbated liver fibrosis upon exposure to CCl4.

10 ctor alpha and CXCL10 but repressed CCL3 and CCL4.

11 id not increase the direct hepatotoxicity of CCl4.

12 xacerbates hepatic fibrosis upon exposure to CCl4.

13 f mRNAs encoding TNF-alpha, IL-10, CCL3, and CCL4.

14 cted intraperitoneally with a single dose of CCl4.

15 he expression of the chemokines MIP-1beta or CCL4.

16 n-1 receptor antagonist (IL-1Ra), IL-18, and CCL4.

17 ocytes are a major source of IFNbeta-induced CCL4.

18 od CXCL4 and CXCL7 and lower levels of blood CCL4.

19 mpaired in their ability to produce CCL3 and CCL4.

20 3 (1.135), IL1alpha (0.952), IL6 (0.931) and CCL4 (0.842).

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

22 Local CCL4, a chemokine liberated by TLR7 agonism, similarly e

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

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

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

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

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

28 antial hepatic fibrosis requires 12 weeks of CCl4 administration.

29 ver regeneration after carbon tetrachloride (CCl4) administration.

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

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

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

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

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

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

36 and interleukin(IL)-1beta in HD11 cells and CCL4 and CCL5 in primary monocytes.

37 uced splenic CD4(+) T cell chemotaxis toward CCL4 and CCL5.

38 (+) T cells in response to the CCR5 ligands, CCL4 and CCL5.

39 By contrast, D. farinae-elicited CCL4 and CCL8 production from pulmonary CD11c(+)CD11b(+)

40 s required their chemotactic factors such as CCL4 and CCR2, the integrations with the monocytes/macro

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

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

43 at 3.5 months of age increases expression of CCL4 and concomitantly protects neuronal dendrites and p

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

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

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

47 g the CCR5-binding chemokine CCL5/RANTES and CCL4 and several members of the tripartite motif-contain

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

49 lease the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-alpha in response to LPS.

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

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

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

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

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

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

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

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

58 secreted higher levels of IL-8, IL-6, CCL3, CCL4, and CCL2 after stimulation with TDM, whereas DC re

59 CCR5 binds the chemokines CCL3, CCL4, and CCL5 and is the major coreceptor for HIV-1 ent

60 r, this motif is partially buried when CCL3, CCL4, and CCL5 are oligomerized; thus, the mechanism by

61 ata and offers a unified mechanism for CCL3, CCL4, and CCL5 assembly into high-molecular-weight, poly

62 Levels of the chemokines CXCL10, CXCL11, CCL4, and CCL5 increased in blood and liver samples from

63 /chemokines, including TNFalpha, IL-6, IL-8, CCL4, and CCL5, by human macrophages stimulated with cel

64 tor of chemokine (C-C motif) ligand (CCL) 3, CCL4, and CCL5, displayed reduced lung damage.

65 chemokines comprising the CCR5 ligands CCL3, CCL4, and CCL5.

66 nic mice also expressed high levels of CCL3, CCL4, and CCL5.

67 CCL3, CCL4, and CXCL10 production was also DR3 dependent, but

68 ), and chemokines (CXCL1, CXCL2, CCL2, CCL3, CCL4, and CXCL10).

69 -gamma-mediated in vitro regulation of CCL3, CCL4, and CXCL10.

70 12, and interleukin 17; the chemokines CCL2, CCL4, and CXCL10; and the growth factors granulocyte-mac

71 nes such as IL-1beta, TNF-alpha, IL-6, CCL3, CCL4, and CXCL11.

72 owing marked reductions in circulating CCL3, CCL4, and CXCL13 levels, and a surge in lymphocytosis du

73 n addition, plasma chemokines such as CCL22, CCL4, and CXCL13 were reduced 40% to 60% after treatment

74 in 17 (IL-17), gamma interferon (IFN-gamma), CCL4, and granulocyte-macrophage colony-stimulating fact

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

76 Serum levels of IFN-gamma, CCL4, and TNF-alpha were significantly increased, wherea

77 enerate inflammatory cytokines (CXCL8, CCL3, CCL4, and TNF-alpha).

78 e tumor associated with increased IFN-gamma, CCL4, and TNF-alpha.

79 otein (MIP)-1alpha/CCL3 (P<0.001), MIP-1beta/CCL4, and vascular endothelial growth factor (VEGF; P<0.

80 g IFNG, TNF, CSF2, chemokines, such as CCL3, CCL4, and XCL1, and modulators of NK cell effector funct

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

82 ior to, or concomitant injections of an anti-CCL4 antibody with MAT.Ang-1 resulted in a significant r

83 ration via production of chemokines CCL3 and CCL4; antibody-based blocking of these chemokines inhibi

84 novel: dimers of the CC chemokines CCL2 and CCL4 are inactive, and the dimer of the CXC chemokine CX

85 -1 (MIP-1), MIP-1alpha (CCL3) and MIP-1beta (CCL4) are chemokines crucial for immune responses toward

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

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

88 d chemokines (interleukin-6, CCL2, CCL3, and CCL4), as well as enhanced mRNA expression of type-I IFN

89 a receptor 1 (IFNAR1) and the beta-chemokine CCL4, as IFNAR1 deficiency and neutralizing antibodies a

90 ion of IFN-gamma, TNF-alpha, CCL2, CCL3, and CCL4, as well as increased airway inflammation and respo

91 of CCL3 binding to CCR5, weak modulators of CCL4 binding, and competitors for CCL5 binding.

92 t of CCR1, the primary receptor for CCL3 and CCL4, blocked cytokine-mediated migration.

93 ced the RSV-mediated induction of CXCL10 and CCL4 but not CCL5.

94 In this study, the repression of CCL3 and CCL4 by IFN-gamma and nitric oxide synthase 2 (NOS2) in

95 Induction of Interferon-beta and Ccl4 by lipoproteins was also partially impaired in cell

96 secretion of BCR-dependent chemokines (CCL3, CCL4) by the CLL cells, both in vitro and in vivo.

97 tes, of chemokine (C-C motif) ligand (CCL)2, CCL4, C-C chemokine receptor (CCR)1, and CCR5, which are

98 we show that CCR5, the receptor for CCL3 and CCL4, can be transiently upregulated on a subset of naiv

99 ukin 18, and interleukin 6; chemokines CCL2, CCL4, CCL11, CCL22, CXCL8, and CXCL10; and T-cell cytoki

100 NF-alpha, IL-1beta, interleukin 12p70; CCL2, CCL4, CCL13, CCL17, CXCL8, CXCL10; and interleukin 2 and

101 cytokines: CL1 (CXCL9, CXCL10, CXCL11, CCL3, CCL4, CCL19, IL-5, IL-12, and IFNgamma), CL2 (TNFalpha,

102 CFII, IL-8, IL-15, VEGFA, LIF, FASL, CXCL11, CCL4, CCL25 and down-regulation of IL-6, IL-9, IL-10, IL

103 cNK-2 induced the expression of CCL4, CCL5 and interleukin(IL)-1beta in HD11 cells and C

104 mmation with elevated plasma levels of Ccl2, Ccl4, Ccl5, and Ccl11 in the myeloid-specific KLF2 knock

105 subset of cytokines (IFN-gamma, CXCL8, CCL2, CCL4, CCL5, and CCL20) correlated with self-reported res

106 regulate production of chemokines, including CCL4, CCL5, and CXCL10, as well as type I interferons, a

107 sociation kinetics, and in the case of CCL3, CCL4, CCL5, CCL24, and XCL1, extremely stable complexes

108 2, IFN-gamma, and TNF) and chemokines (CCL3, CCL4, CCL5, CXCL9, and CXCL10).

109 ed concentrations of the NK cell attractants CCL4, CCL5, CXCL9, and CXCL10; all levels in synovial fl

110 rs to be a key cytokine that limits the CCR5-CCL4/CCL5 axis during inflammatory settings.

111 ere highly associated with AMR (P < 5 x 10): CCL4, CD160, CCL3, XCL1, CRTAM, FCRL3, STARD4, TNFRSF9.

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

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

114 ses and promoted CLL cell survival, CCL3 and CCL4 chemokine secretion, and downregulation of BCL6, th

115 associated with immune suppression, but with CCL4 (chemokine [C-C motif] ligand 4)-mediated recruitme

116 tion and transcript accumulation of CCL3 and CCL4 chemokines, both of which are induced by FGFR3 acti

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

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

119 In CCl4 -cirrhotic rats, terutroban reduced liver fibrosis

120 kines (TNFalpha, IL-6) and chemokines (CCL2, CCL4, CXCL1, CXCL2, CXCL10) are critically regulated by

121 receptor-signaling pathways, including CCL3, CCL4, CXCL10, CXCL11, ITGA4, ITGB1, ADAM28, and ADAMDEC1

122 M1- and M2-associated genes, including Il6, Ccl4, Cxcl2, Arg1, Chi3l3, Ccl11, and Il10, respectively

123 ce showed marked upregulation of CCL2, CCL3, CCL4, CXCL2, CXCL10, TNFalpha, and IL-1beta compared to

124 arameters, seven chemokines/cytokines, CCL3, CCL4, CXCL9, CXCL10, CXCL11, IL-10 and IFN-gamma, and ge

125 DSC that produce increased IL-23, IL-1b, and CCL4 cytokines compared to Mo-MDSC from healthy controls

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

127 Only MIP-1 chemokines, including Ccl3 and Ccl4, displayed peak expression 24 h after light exposur

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

129 0.06 Gg y(-1)) but only 8% (3-22%) of global CCl4 emissions during these years.

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

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

132 vere photoreceptor cell death, and increased Ccl4 expression compared with Abca4(-/-)Rdh8(-/-) mice.

133 infection of DCs resulted in CCL2, CCL3, and CCL4 expression, which was abrogated after RIG-I and MDA

134 NP tissue samples showed that CCL3, but not CCL4, expression correlated positively with the grade of

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

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

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

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

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

140 CCl4-gavaged mice were also injected with attenuated ade

141 Mice lacking CCR5 or treated with an mAb to CCL4 had impaired infiltration of inflammatory cells to

142 Mice lacking CCR5 or treated with a mAb to CCL4 had more Tregs in the thymus prior to and during in

143 Although blocking CCL3 and CCL4 has no effect on primary CD8(+) T cell responses, i

144 toplasmosis, mice lacking CCR5 or endogenous CCL4 have a reduced number of Tregs in the lungs, which

145 and IFN-gamma and chemokines CCL2, CCL3, and CCL4 have been associated with disease severity, endothe

146 f Th2 (IL-13, CCL17, eotaxin-1/CCL11, CCL13, CCL4, IL-10), Th1 (CXCL10, CXCL11) and Th1/Th17/Th22 (IL

147 ing factor (G-CSF)/CSF3, CXCL1, CXCL5, CCL2, CCL4, IL-6, tumor necrosis factor alpha (TNF-alpha), IL-

148 oinflammatory cytokines (CXCL1, CXCL2, CCL3, CCL4, IL6, and CSF3), silencing of major inflammatory in

149 etory activating phenotype (ASAP), releasing CCL4, IL8, VEGF, and TNFalpha from treated tumor cells.

150 IFN-gamma repressed CCL3 and CCL4 in a signal transducer and activator of transcripti

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

152 nistic insight on the regulation of CCL3 and CCL4 in mouse macrophages and during S. typhimurium oral

153 MK2 signaling regulated chemokines CCL3 and CCL4 in murine calvarial tissue.

154 and a significant increase in the levels of CCL4 in peritoneal lavage fluid.

155 ofiles based on gp130, SH2D1B, TNFalpha, and CCL4 in plasma exosomes may be used to predict on-going

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

157 Specifically, Tregs produced both CCL3 and CCL4 in response to stimulation, and production of these

158 signaling differentially regulated CCL3 and CCL4 in the hematopoietic and nonhematopoietic compartme

159 AB3IP), 12q21.1 (GLIPR1L1), and 17q12 (ERBB2/CCL4) in SDC.

160 one IL-17 and IFNalpha increased in smokers, CCL4 increased in never smokers and CCL5 and CXCL10 redu

161 ion with one of the CCR5 ligands, MIP-1beta (CCL4), increased their resistance against HIV.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

180 or etanercept inhibits carbon tetrachloride (CCL4)-induced fibrogenesis in an ERG-dependent manner in

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

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

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

184 6 mice with or without carbon tetrachloride (CCl4)-induced liver fibrosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

198 g liver tissue damage and regeneration after CCl4 intoxication.

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

200 CCL4 is associated with cellular neovascularization, whe

201 th PegIFN/RBV, while baseline serum level of CCL4 is the only predictor for NR in GT-1 CHC patients w

202 plasma IL-1alpha, IL-12p40, CCL2, CCL3, and CCL4 levels.

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

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

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

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

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

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

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

210 rane protein (LAMP), low levels of MIP1-beta/CCL4, MIG/CXCL9, and severe defect of interleukin-12 (IL

211 e promoters, the human CCL3 (MIP-1alpha) and CCL4 (MIP-1beta), were transfected into human chondrocyt

212 okines Cxcl2 (MIP-2), Ccl3 (MIP-1alpha), and Ccl4 (MIP-1beta).

213 roduction of high levels of CCL3/MIP-1alpha, CCL4/ MIP-1beta, and CCL5/RANTES but not of CXCL12/SDF-1

214 ctor alpha (TNF-alpha), CCL3/MIP-1alpha, and CCL4/MIP-1beta production and lower neutrophil recruitme

215 0.05) 0.02 muM HagB-induced CCL3/MIP-1alpha, CCL4/MIP-1beta, and TNFalpha responses.

216 0, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL7/MCP-3, and CCL20/MIP3alpha protein

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

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

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

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

221 of five biologically relevant genes (CXCL11, CCL4, MS4A7, MS4A6A, and FCGR3A) indicative of endotheli

222 o activation of an adaptive immune response, CCL4-neutralized and CCR5(-/-) mice resolved infection m

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

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

225 Intratumoral injection of CCL4 or CCL5 increased tumor-infiltrating Tregs, and def

226 diated neutralization of CCL2, but not CCL3, CCL4 or CCL5, prevented NK cell recruitment to the senes

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

228 Elimination of CD4+ T cells or blockade of CCL4 or IL-17 abrogated the increase in tumor formation

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

230 of microglia or the presence of CCR5 ligand CCL4 or p38 MAPK inhibitors.

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

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

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

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

235 is not mediated by IL-10, TGF-beta, CTLA-4, CCL4, or adenosine and relies on interference with very

236 oss all classes, and a reduction in CCL3 and CCL4 plasma levels was noted in responding patients.

237 CCl4 produced similar fibrosis and necroinflammation and

238 m Ccl3-/- mice, which are also deficient for CCL4 production, did not promote migration.

239 BMDMs, IFN-gamma and NOS2 repressed CCL3 and CCL4 production.

240 to LL-37 for chemotaxis, degranulation, and CCL4 production.

241 chondrocytes were transfected with CCL3 and CCL4 promoter constructs, pNF-kappaB reporter, and NF-ka

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

243 [chemokine (C-C motif) ligand 3], MIP-1beta/CCL4, RANTES (regulated on activation, normal T-cell exp

244 ngly, secretion of CXCL1, CXCL2, CCL2, CCL3, CCL4, RANTES, and TNF-alpha, but not IL-1alpha, IL-1beta

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

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

247 ficiency and neutralizing antibodies against CCL4, respectively, abolish the neuroprotective effects.

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

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

250 (51D) attenuated hepatocyte damage caused by CCl4, TGF-beta1, and chemokine production.

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

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

253 -1beta, IL-10, IL-17, IFN-gamma, CCL2, CCL3, CCL4, TNF-alpha, G-CSF, GM-CSF, fibroblast growth factor

254 acellular levels of the key cytokines (CCL3, CCL4, TNFalpha) identified by the mRNA analysis.

255 genes, we identified multiple genes (gp130, CCL4, TNFalpha, SH2D1B, CAV1, atypical chemokine recepto

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

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

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

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

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

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

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

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

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

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

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

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

268 CCl4 treatment enhances degeneration and DNA damage in N

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

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

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

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

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

274 damage resulting from carbon tetrachloride (CCl4) treatment.

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

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

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

278 2F1 complexes in C/EBPalpha-S193D mice after CCl4 treatments.

279 nd acceleration of liver proliferation after CCl4 treatments.

280 d liver injury and proliferation after acute CCl4 treatments.

281 Fund Chronic Lymphocytic Leukemia 4 (UK LRF CCL4) trial that compared chlorambucil and fludarabine w

282 els of IL-6, IL-8, chemokine ligand (CCL) 3, CCL4, tumor necrosis factor, and IL-1beta, factors assoc

283 CXCL16 and CCL4, unique chemokine ligands for CXCR6 and CCR5, respe

284 ture DC (iDC)-attracting chemokines CCL3 and CCL4 upon exposure to tumor cells or the additional infl

285 cerebral and dermal MVECs, and CXCL8, CCL3, CCL4, VCAM-1, and cyclooxygenase 2 (COX-2) in cerebral M

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

287 CCL4 was detected on the tumor vasculature in a majority

288 In addition, baseline serum level of CCL4 was found to be the only independent factor for NR

289 from 4 genes of gp130, SH2D1B, TNFalpha, and CCL4 was significantly higher in the AMR than the CMR (P

290 ukotrienes, TNFalpha, CXCL8, CCL2, CCL3, and CCL4, was almost completely inhibited by CE.

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

292 Tregs deficient for expression of CCL3 and CCL4 were impaired in their ability to suppress experime

293 Levels of VEGF and CCL4 were increased in CSF of GBM and correlated with th

294 ine serum levels of CXCL10, CXCL11, CCL3 and CCL4 were significantly higher in NR group while compari

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

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

297 2 per thousand (CHCl3) and 0.4 per thousand (CCl4), which are only about twice as large as 0.1 per th

298 his complex enhances the release of CCL3 and CCL4, which facilitate additional interaction with naive

299 , clade H (SERPINH1) and chemokine ligand 4 (CCL4), while exploratory gene ontology (GO) analyses rev

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