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 ted via the diffusion of chemokines CCL3 and CCL4.

6 mpaired in their ability to produce CCL3 and CCL4.

7 iding hazardous chlorinated solvents such as CCl4.

8 we performed chronic treatments of mice with CCl4.

9 (+)-galactosamine and lipopolysaccharides or CCl4.

10 exacerbated liver fibrosis upon exposure to CCl4.

11 ctor alpha and CXCL10 but repressed CCL3 and CCL4.

12 id not increase the direct hepatotoxicity of CCl4.

13 xacerbates hepatic fibrosis upon exposure to CCl4.

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

15 1, CXCL7 and CXCL8 and lower blood levels of CCL4.

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

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

18 3 (1.135), IL1alpha (0.952), IL6 (0.931) and CCL4 (0.842).

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

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

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

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

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

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

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

26 antial hepatic fibrosis requires 12 weeks of CCl4 administration.

27 ver regeneration after carbon tetrachloride (CCl4) administration.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 hemokines C-C motif chemokine ligand (CCL)2, CCL4, and C-X-C motif chemokine ligand 10 in CB(2)(-/-)

57 10, C-C motif chemokine ligand [CCL]2, CCL3, CCL4, and CCL13) in nasal mucosal fluid, without causing

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

59 mor necrosis factor alpha (TNF-alpha), CCL3, CCL4, and CCL20, their HIV-1 reactivation capacity was a

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

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

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

63 IL13, chemokine (C-C motif) ligand (CCL) 3, CCL4, and CCL5 were higher in the HCC group and associat

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

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

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

67 and myeloid chemotaxis and activation (CCL3, CCL4, and CDCP1), and mucosal immune dysregulation (IL-1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 he macrophage inflammatory proteins CCL3 and CCL4 as well as resistin, which augments monocyte-endoth

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

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

88 expression of the T cell chemokines CCL3 and CCL4, as well as CD86 and ICAM1.

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

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

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

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

93 -1beta, CXCL1, CXCL5, IL-3, CXCL2, CCL3, and CCL4, but decreased levels of IL-4, CXCL9, and CXCL10 co

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 .) and decreased chemokine production (CCL2, CCL4, CCL11).

100 reatment, the baseline levels of CCL1, CCL2, CCL4, CCL11, and CXCL11 and mycobacterial Ag-stimulated

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

102 the peritoneal cavity and serum (CCL2, CCL3, CCL4, CCL11, CXCL1, CXCL2, CXCL5, CXCL9, G-CSF, GM-CSF,

103 icantly diminished production of CCL1, CCL2, CCL4, CCL11, CXCL2, CXCL9, and CXCL10 in comparison with

104 icantly diminished production of CCL1, CCL2, CCL4, CCL11, CXCL9, CXCL10, and CXCL11 in comparison wit

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

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

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

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

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

110 IL-10, IL-12(p40), IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL11, G-CSF, GM-CSF and TNF-alpha.

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

112 2, IFN-gamma, and TNF) and chemokines (CCL3, CCL4, CCL5, CXCL9, and CXCL10).

113 o express T cell-recruiting chemokines CCL3, CCL4, CCL5.

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

115 tokines and other markers (e.g., CCL2, CCL3, CCL4, CD137 and ANG-1 levels) compared with untreated sp

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

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

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

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

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

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

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

123 In CCl4 -cirrhotic rats, terutroban reduced liver fibrosis

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

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

126 Six chemokines (CCL2, CCL3, CCL4, CXCL8, CXCL10 and CX3CL1) were associated with inc

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

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

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

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

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

132 0.06 Gg y(-1)) but only 8% (3-22%) of global CCl4 emissions during these years.

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

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

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

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

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

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

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

140 zygotes to elicit anti-HIV functions such as CCL4, gamma interferon (IFN-gamma), and CD107a expressio

141 L2, KIR2DL3, and KIR3DL1 NK cells to produce CCL4, gamma interferon (IFN-gamma), and/or CD107a were a

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

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

144 CCl4-gavaged mice were also injected with attenuated ade

145 ristic of effector memory T cells, including CCL4, GNLY and NKG7.

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

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

148 o autologous HIV-infected cells by producing CCL4, IFN-gamma, and CD107a.

149 uency of production by spiKIR(+) NK cells of CCL4, IFN-gamma, and/or CD107a.

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

151 nflammatory markers, such as Il17f, Tnfsf11, Ccl4, Il1a, Ccr2, Il4, Il5, and Csf2 in the retina, and

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

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

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

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

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

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

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

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

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

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

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

163 d IFIH1 in the Fayoumi versus IL8, CAMP, and CCL4 in the Leghorn.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

189 6 mice with or without carbon tetrachloride (CCl4)-induced liver fibrosis.

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

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

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

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

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

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

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

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

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

199 ta [MIP-1beta]/C-C motif chemokine ligand 4 [CCL4], interferon gamma-induced protein-10 [IP-10]/C-X-C

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

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

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

203 g liver tissue damage and regeneration after CCl4 intoxication.

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

205 CCL4 is associated with cellular neovascularization, whe

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

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

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

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

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

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

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

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

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

215 , CCL5 [C-C motif chemokine ligand 5], CCL7, CCL4, MIF [macrophage migration inhibitory factor]), clu

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

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

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

219 0.05) 0.02 muM HagB-induced CCL3/MIP-1alpha, CCL4/MIP-1beta, and TNFalpha responses.

220 0, CCL5/RANTES, CCL11/eotaxin-1, CCL2/MCP-1, CCL4/MIP-1beta, CCL7/MCP-3, and CCL20/MIP3alpha protein

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 beta, and TNF-alpha) and chemokine (CCL3 and CCL4) production.

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

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

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

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

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

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

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

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

249 (51D) attenuated hepatocyte damage caused by CCl4, TGF-beta1, and chemokine production.

250 1A has a lower binding affinity for CCL2 and CCL4 than ACKR2-WT.

251 (TNF-alpha), CXCL1, CXCL2, CXCL10, CCL3, and CCL4 than infected type 1 or type 3 ILCs.

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

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

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

271 g unit at baseline and 1 week after the last 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 CXCL16 and CCL4, unique chemokine ligands for CXCR6 and CCR5, respe

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

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

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

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

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

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

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

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

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

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

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

294 increased RNA expression of Ccl2, Ccl3, and Ccl4, when compared with adult mice, at 72 h postinfecti

295 2 per thousand (CHCl3) and 0.4 per thousand (CCl4), which are only about twice as large as 0.1 per th

296 Among these is CCL4, which binds and blocks CCR5, the coreceptor for HI

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

298 to activate naive CD8(+ )T cells to produce Ccl4, which induces microglia to produce a key LGG growt

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