ライフサイエンスコーパス: p-dioxin

1 effects of TCDD (2,3,7,8 tetrachlorodibenzo-p-dioxin).

2 ivation by TCDD (2, 3,7,8-tetrachlorodibenzo-p-dioxin).

3 as TCDD (dioxin, 2,3,7,8-tetrachlorodibenzo-p-dioxin).

4 ve congeners of tetra- to octachloro-dibenzo-p-dioxins).

5 ynthetic chemical 2,3,7,8-tetrachlorodibenzo-p-dioxin.

6 d the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin.

7 from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

8 e toxic compound 2,3,7,8,-tetrachlorodibenzo-p-dioxin.

9 nic properties of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

10 nt and AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin.

11 al enzyme inducer 2,3,7,8-tetrachlorodibenzo-p-dioxin.

12 lcholanthrene and 2,3,7,8-tetrachlorodibenzo-p-dioxin.

13 of agonists like 2,3, 7,8-tetrachlorodibenzo-p-dioxin.

14 aminants such as 2,3,7, 8-tetrachlorodibenzo-p-dioxin.

15 in-like compound, 2,3,7,8-tetrachlorodibenzo-p-dioxin.

16 racterized toxicants polychlorinated dibenzo-p-dioxins.

17 for the formation of polybrominated dibenzo-p-dioxins.

18 tochemically to form polychlorinated dibenzo-p-dioxins.

19 pb-level yields of 1,3,6,8-tetrabromodibenzo-p-dioxin (1,3,6,8-TeBDD) through direct condensation.

20 1-, 2-MCDD), 1,6-, 1,9-, 1,3-dichlorodibenzo-p-dioxin (1,6-, 1,9-, 1,3-DCDD), 4-monochlorodibenzofura

21 zo-p-dioxin (DD), 1- and 2-monochlorodibenzo-p-dioxin (1-, 2-MCDD), 1,6-, 1,9-, 1,3-dichlorodibenzo-p

22 , benzo(a)pyrene, 2,3,7,8-tetrachlorodibenzo-p-dioxin, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin, and

23 l be as toxic as 2,3,7,8-tetrachloro-dibenzo-p-dioxin (2378-TCDD), a compound reputed as one of the m

24 also increased by 2,3,7,8-tetrachlorodibenzo-p-dioxin, an AhR activator, through the AhR site.

25 ment management alternatives for the dibenzo-p-dioxin and -furan (PCDD/F) contaminated Grenland fjord

26 a sediment capping strategy for the dibenzo-p-dioxin and -furan contaminated Grenland fjord system i

27 AHR ligands (i.e. 2,3,7,8-tetrachlorodibenzo-p-dioxin and alpha-naphthoflavone) neither induced apopt

28 AhR activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin and benzo[a]pyrene.

29 ost PCDD/Fs (1.0 pg/g for heptachlorodibenzo-p-dioxin and heptachlorodibenzofuran and 2.0 pg/g for oc

30 o be inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin and hypoxia.

31 nd 2-azido-3-[(125)I]iodo-7,8-dibromodibenzo-p-dioxin and liver cytosol isolated from hepatocyte-spec

32 ogical effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin and related compounds.

33 h 2-azido-3-[(125)I]iodo-7, 8-dibromodibenzo-p-dioxin and velocity sedimentation analysis using 2,3,7

34 yl ethers (PBDEs) and polybrominated dibenzo-p-dioxins and -furans (PBDDs/Fs) from a common flue gas

35 Polychlorinated dibenzo-p-dioxins and -furans (PCDD/Fs) are persistent organic p

36 biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and -furans (PCDD/Fs).

37 for determination of polychlorinated dibenzo-p-dioxins and -furans (PCDDs/Fs) emissions from municipa

38 -furans, and all 210 polychlorinated dibenzo-p-dioxins and -furans present in the flue gas at levels

39 ,7,8-Br-substituted tri- to octabromodibenzo-p-dioxins and -furans, and all 210 polychlorinated diben

40 operator18PCBs) and polychlorinated dibenzo-p-dioxins and dibenzofurans ( summation operator17PCDD/F

41 dies the formation of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) by de novo synthes

42 ields of formation of polybrominated dibenzo-p-dioxins and dibenzofurans (PBDD/Fs) from the polybromi

43 as and aerosol phase polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and dioxin like po

44 ic pollutants, i.e., polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) and polycyclic aro

45 Polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) are a group of com

46 biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) are persistent org

47 rocarbons (PAHs) and polychlorinated-dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) from incineration

48 e pollution trend of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in the Baltic Sea

49 trends of sources of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) in the Baltic Sea

50 ers of tetra- to octapolychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs) vapors were studie

51 to be precursors of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), a rigorous assess

52 Concentrations of polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), polychlorinated b

53 biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins and dibenzofurans (PCDD/Fs).

54 of potentially toxic polyhalogenated dibenzo-p-dioxins and dibenzofurans (PXDD/Fs and PBDD/Fs).

55 ysis of mixed brominated/chlorinated dibenzo-p-dioxins and dibenzofurans (PXDD/PXDFs, X = Br and Cl)

56 mixed bromo-/chloro- and polybromo-) dibenzo-p-dioxins and dibenzofurans in the simulated burn study

57 ousands of different polyhalogenated dibenzo-p-dioxins and dibenzofurans that could negatively impact

58 d bioaccumulation of polychlorinated dibenzo-p-dioxins and dibenzofurans, hexachlorobenzene, and octa

59 ated diphenyl ethers, polybrominated dibenzo-p-dioxins and dibenzofurans, polybrominated biphenyls an

60 omatic hydrocarbons, polychlorinated dibenzo-p-dioxins and dibenzofurans, polychlorinated biphenyls,

61 the present study, 12 polybrominated dibenzo-p-dioxins and furans (PBDD/Fs) were analyzed by gas chro

62 Polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) and dioxin-like polychlor

63 rs and fragrances and for tetrachlorodibenzo-p-dioxins and furans, which follow SOT based on the Pois

64 ing to, for example, polychlorinated dibenzo-p-dioxins and other organic pollutants is already high.

65 talytic formation of polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans (PCDD/Fs) fr

66 synthesis of PCDD/F (polychlorinated dibenzo-p-dioxins and polychlorinated dibenzofurans, also known

67 ental AHR ligands 2,3,7,8-tetrachlorodibenzo[p]dioxin and benzo[a]pyrene mimic this effect.

68 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expression in reporter gene ass

69 o-p-dioxin, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin, and octachlorodibenzo-p-dioxin is studied usin

70 ic bud inhibitor, 2,3,8,7-tetrachlorodibenzo-p-dioxin, and restored ventral prostate morphogenesis wh

71 of molecules like 2,3,7,8-tetrachlorodibenzo-p-dioxin as well as regulation of normal liver developme

72 inhibit agonist (2,3,7,8-tetrachlorodibenzo-p-dioxin) binding, nuclear translocation of AHR, and ago

73 specific agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin but were absent in AhR(d) mice.

74 ototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin can affect G1 phase progression in cultured cel

75 agonists, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, cause severe toxic effects, ITE exhibits no to

76 receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin causes altered gene expression and toxicity.

77 a determinant of 2,3,7,8-tetrachlorodibenzo-p-dioxin concentration and with prospective cohort data

78 the PCDD (5% of 2,3,7,8- tetrachlorodibenzo-p-dioxin) concentrations in the rural and background atm

79 ished AhR ligand 2,3,7,8,-tetrachlorodibenzo-p-dioxin, curcumin inclusion resulted in AhR nuclear tra

80 TCS led to formation of 2,8-dichlorodibenzo-p-dioxin (DCDD).

81 Dibenzo-p-dioxin (DD) sorption from water by DODA-SWy-2 was comp

82 ed and nonchlorinated DD/Fs comprise dibenzo-p-dioxin (DD), 1- and 2-monochlorodibenzo-p-dioxin (1-,

83 ene promoter in a 2,3,7,8-tetrachlorodibenzo-p-dioxin -dependent manner.

84 hancer in a TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin)-dependent fashion in vivo, and Med220 LXXLL mo

85 availability of aged polychlorinated dibenzo-p-dioxin/dibenzofurans (PCDD/Fs) in two soils.

86 e and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) among veterans of Operation Ranch Hand

87 common practice for polychlorinated dibenzo-p-dioxin (dioxin) and related compounds.

88 compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) and the developmental closure of a fet

89 a central role in 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) hepatotoxicity, regulation of xenobiot

90 e and exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) in veterans of Operation Ranch Hand, t

91 d is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin) via the aryl hydrocarbon receptor (AHR

92 with exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), and vascular remodeling of the develo

93 ollutants such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin), in the adaptive up-regulation of xeno

94 corresponding to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin)-inducible genes from mouse Hepa-1 cell

95 vironmental toxin 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

96 to the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

97 ollow exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

98 and teratology of 2,3,7,8-tetrachlorodibenzo-p-dioxin (dioxin).

99 The pollutant, 2,3,7,8-tetrachlorodibenzo-p-dioxin ("dioxin"), has been implicated in the etiology

100 ental toxin TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin, dioxin) produces diverse toxic effects includi

101 ells treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin during hypoxia and normoxia.

102 tagonist reversed 2,3,7,8-tetrachlorodibenzo-p-dioxin-elicited suppression of early B and pro-B cells

103 mpetes with 2,3,7,8-[(3)H]tetrachlorodibenzo-p-dioxin for binding to human, murine, and fish AHRs, th

104 , NOx, heavy metals, polychlorinated dibenzo-p-dioxins/furan (PCDD/F), polycyclic aromatic hydrocarbo

105 iphenyls (PCBs), and polychlorinated dibenzo-p-dioxins/furans (PCDD/Fs) to resident/migratory biota w

106 otent AhR agonist 2,3,7,8-Tetrachlorodibenzo-p-dioxin had no effect on TGF-beta1 expression, indicati

107 gands, such as 2,3,7, 8-tetrachlorodibenzeno-p-dioxin, have been shown to modify cell proliferation a

108 portions of 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin (HpCDD), a known product of the dechlorination

109 oth forskolin and 2,3,7,8-tetrachlorodibenzo-p-dioxin increased COX-2 mRNA in a dose-dependent manner

110 ion by its ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin induced functional T(reg) cells that suppressed

111 resistant to all 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxic responses that we examined, inclu

112 Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) induces cleft palate and hydronephrosis in mic

113 echanism by which 2,3,7,8-tetrachlorodibenzo-p-dioxin is able to disrupt epidermal homeostasis and id

114 hlorodibenzo-p-dioxin, and octachlorodibenzo-p-dioxin is studied using daily global emissions from ve

115 ants like dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin) leads to many adverse biological effects, incl

116 n genes exhibited 2,3,7,8-tetrachlorodibenzo-p-dioxin-mediated regulation, although there were signif

117 articular case of dioxins, octachlorodibenzo-p-dioxin (OCDD) was the most abundant PCDD/F congener.

118 t of the dechlorination of octachlorodibenzo-p-dioxin (OCDD), and other known dechlorination products

119 arbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin on long-term self-renewal of murine hematopoiet

120 ion of the AhR by 2,3,7,8-tetrachlorodibenzo-p-dioxin or certain polycyclic aromatic hydrocarbons can

121 by which dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin or TCDD)-mediated formation of the aryl hydroca

122 Polybrominated dibenzo-p-dioxins (PBDD) are emerging environmental pollutants w

123 Brominated and mixed halogenated dibenzo-p-dioxins (PBDDs and PXDDs) may well be as toxic as 2,3,

124 High levels of polybrominated dibenzo-p-dioxins (PBDDs) have been found in Baltic Sea biota, w

125 amination profiles of polybrominated dibenzo-p-dioxins (PBDDs), dibenzofurans (PBDFs), diphenyl ether

126 Polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF) are ubiquitous

127 the determination of polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF) in environment

128 cluding highly toxic polychlorinated dibenzo-p-dioxins (PCDD) and dibenzofurans (PCDF).

129 n and destruction of polychlorinated dibenzo-p-dioxins (PCDD) and polychlorinated dibenzofurans (PCDF

130 Emissions including polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCD

131 ished to investigate polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCD

132 ompounds (VOCs), and polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCD

133 3,7,8-chlorine-substituted polychlorodibenzo-p-dioxins (PCDDs) and polychlorodibenzofurans (PCDFs).

134 Although polychlorinated dibenzo-p-dioxins (PCDDs) quantified in the samples accounted fo

135 mpared with those of polychlorinated dibenzo-p-dioxins (PCDDs), dibenzofurans (PCDFs), and biphenyls

136 Our research reports polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs)

137 biphenyls (PCBs) and polychlorinated dibenzo-p-dioxins (PCDDs), solubility-derived KPDMSw increased l

138 nzo-p-dioxin (TCDD), polychlorinated dibenzo-p-dioxins (PCDDs)], furans, polychlorinated biphenyls (P

139 sequent formation of polychlorinated dibenzo-p-dioxins, polychlorinated dibenzofurans (PCDD/F, dioxin

140 (PBDEs), and mixed monobromo/chloro dibenzo-p-dioxins (PXDDs) and dibenzofurans (PXDFs) were determi

141 canonical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin resulted in concomitant recruitment of carbamoy

142 P450 induction by 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly enhanced the antiproliferative ef

143 h-affinity ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin significantly suppressed the generation of earl

144 nmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD = dioxin) has been shown to increase the

145 standard and pure 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (normalized at 0.1 mug/kg TEQ) and acqui

146 ated at 162 ng/kg 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (range: 15-672), which is equivalent to

147 ) or E2 plus 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) (reference) or 25 microM diindolylmethan

148 D) completely inhibited 2,3,7, 8-tetrachloro-p-dioxin (TCDD) -dependent activation of a xenobiotic re

149 n animal studies, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters glucose transport and increases s

150 by the pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) alters the in vivo distribution and freq

151 The potency of tetrachlorodibenzo-p-dioxin (TCDD) and 18 polycyclic aromatic hydrocarbons

152 eing observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and also microbiota-derived AhR ligands

153 se proteins bind 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and are able to bind dioxin response ele

154 a1c1c7 cells with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and Erk kinase inhibitor PD98059, U0126,

155 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon receptor (AhR

156 k assessments for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other dioxins rely on estimates of e

157 t is activated by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other related compounds, leading to

158 or through which 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds cause altered gene

159 The effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related compounds occur via the aryl

160 toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and related environmental contaminants.

161 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related halogenated aromatic hydroca

162 CYPLucR(+/-) mice, 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD) and several other aryl hydrocarbon recep

163 ys, activities of 2,3,7,8-tetrochlorodibenzo-p-dioxin (TCDD) and six synthetic flavonoids were evalua

164 n serum levels of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the occurrence of diabetes mellitus

165 gh the effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are mediated through binding and activat

166 R agonist such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt G1 phase cell cycle progress

167 tor (AhR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) can disrupt the regenerative process, as

168 ental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes a wide range of toxic, teratogeni

169 h the AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) compromises the competitive reconstituti

170 a model to study 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) developmental toxicity, it is essential

171 yperactivation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during zebrafish (Danio rerio) developme

172 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exerts its toxic action via the aryl hyd

173 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exhibits antiestrogenic properties, incl

174 tigations linking 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure in humans with coronary artery

175 RNT2b and zfAHR2, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure leads to a significant inductio

176 erious effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure.

177 1) compete with 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) for binding to the AhR; 2) inhibit TCDD-

178 with exposure to 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) for women who resided near Seveso, Italy

179 ntal contaminant 2,3,7,8,-tetrachlorodibenzo-p-dioxin (TCDD) has been shown to cause thymic atrophy i

180 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal developmen

181 by the AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in a concentration-dependent manner.

182 ally inhibited by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in adult zebrafish and have used this in

183 d is inducible by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the human breast adenocarcinoma cell

184 potent AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) induced Cbr1 expression in Ahr(+/-) and

185 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in

186 tly reported that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) inhibits epidermal growth factor (EGF) w

187 )pyrene (BaP) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) interact with the aryl hydrocarbon recep

188 ly concluded that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a human carcinogen.

189 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a multispecies reproductive toxicant,

190 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminan

191 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent environmental contaminan

192 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a ubiquitous environmental contaminan

193 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread environmental contaminan

194 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a widespread industrial environmental

195 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental toxicant known to in

196 owing exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is based upon the identities of the amin

197 hydrocarbons, of which 2,3,7, 8-tetrachloro-p-dioxin (TCDD) is the prototype compound, elicit a vari

198 otent AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) leads to a significant decline in the pe

199 toxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on T cells in vivo have been well charac

200 ypical AhR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the expression of cytochrome P450 (CY

201 arbon receptor by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the formation of the epicardium

202 receptor (AHR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) prevents the proper formation of craniof

203 receptor (AhR) by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) resulted in loss of the programmed cell

204 ental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) results in a variety of pathological les

205 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) suppresses many immune responses, both i

206 n the presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) than vehicle and was also Arnt-dependent

207 d previously that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) up-regulates Fas and FasL in immune cell

208 highly induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) via the aryl hydrocarbon receptor.

209 B[a]P) as well as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were docked to multiple models of rat, h

210 proliferation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) were studied in the human-derived LNCaP

211 encies (RePs) of 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD), 2,3,4,7,8-pentachloro-dibenzofuran, 2,3

212 eceptor (AhR) by 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent agonist of AhR, induces a mark

213 Whereas 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), a potent agonist of AhR, induces a rapi

214 ntial stressor is 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a powerful toxicant known to disturb to

215 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototypical Ahr agonist, had an indu

216 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental contaminant,

217 pollutants, e.g., 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), activate the aryl hydrocarbon receptor

218 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an aryl hydrocarbon receptor (AhR) agon

219 Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental pollutant, has been sh

220 ns (PAH), such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), and mediates their toxicity.

221 c ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), associates with the AHR nuclear translo

222 unresponsive to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD), basal CYP1B1 mRNA and protein were expr

223 or) ligands such as 2,3,7,8-tetrachlodibenzo-p-dioxin (TCDD), beta-naphthoflavone, and benzo[a]pyrene

224 ioxins, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), causes a wide array of toxicities in ve

225 r (AHR) agonist, 2,3,7,8-tetracholorodibenzo-p-dioxin (TCDD), causes increases in both hepatocytic an

226 d rtAHR2beta bind 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dimerize with rainbow trout ARNTb (rtAR

227 after exposure to 2,3,7,8-tetrachlorodibezo-p-dioxin (TCDD), geldanamycin (GA), or the protease inhi

228 nobiotics such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), has more recently attracted the attenti

229 pical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in utero and via suckling.

230 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily produced via industrial pr

231 st potent ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), leads to immune suppression in mice.

232 tions of dioxins [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), polychlorinated dibenzo-p-dioxins (PCDD

233 otoxic effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), possibly by rendering cells less respon

234 ocarbon receptor, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), produced a similar induction of P-glyco

235 hracene (DMBA) or 2,3,5,7-tetrachlorodibenzo-p-dioxin (TCDD), was inhibited by cotreatment with fluas

236 yrene [B(a)P] and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which have been shown to act as endocri

237 n receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), which is not metabolized, did not affec

238 ational change of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-bound AhR.

239 the regulation of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced apoptosis in thymic T cells.

240 hR also decreased 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced CYP1A1 protein, CYP1A1-dependent

241 spirin 2 inhibited 2,3,7,8-tetrachlordibenzo-p-dioxin (TCDD)-induced cytochrome P450 (CYP) enzyme act

242 hibited DMBA- and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced enzyme activity and CYP1A1, 1A2,

243 Activation of AhR induced tetrachlorodibenzo-p-dioxin (TCDD)-inducible poly(ADP-ribose) polymerase (T

244 the LPS-enhanced 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-mediated induction of CYP1A1 in thymus o

245 ental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

246 ototypical ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

247 yrene (B[a]P) and 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD).

248 ligands, such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

249 potent carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

250 petition with [3H]2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

251 tor (AhR) ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

252 otent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

253 the AHR agonist, 2,3,7,8-tetra-chlorodibenzo-p-dioxin (TCDD).

254 utants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

255 g ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

256 h receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

257 toxins such as 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

258 compounds such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

259 chieved with only 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

260 ponses induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

261 CYP1A1 induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

262 ptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

263 inants, including 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

264 ding, typified by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

265 n receptor ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

266 racene (DMBA) or 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

267 ofuran (TCDF) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

268 ntal contaminant 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

269 that observed for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

270 its affinity for 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

271 r the AHR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

272 ligands for AhR [2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)], CAR [6-(4-chlorophenyl)imidazo[2,1-b][

273 nmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) causes numerous and diverse toxi

274 in and carcinogen 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin) include a wasting syndrome assoc

275 factor that binds 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

276 rocarbons such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin).

277 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is known to induce rapid infl

278 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is a toxic environmental contami

279 stress induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is poorly understood.

280 Dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin, TCDD) is a carcinogenic and highly toxic indus

281 bility of dioxin (2,3,7,8-tetrachlorodibenzo[p]dioxin, TCDD) to promote epigenetic transgenerational

282 ntaminant dioxin (2,3,7,8-tetrachlorodibenzo-p-dioxin; TCDD).

283 In response to 2,3,7,8-tetrachlorodibenzo-p-dioxin, the AHR.

284 during hypoxia by 2,3,7,8-tetrachlorodibenzo-p-dioxin, the induction of P4501A1 protein was reduced b

285 mically generating 2,3,7,8-tetrabromodibenzo-p-dioxin, the most toxic brominated dioxin congener.

286 tivity by FICZ or 2,3,7,8-tetrachlorodibenzo-p-dioxin, thereby subsequently elevating intracellular l

287 iscrepancies between polychlorinated dibenzo-p-dioxin to polychlorinated dibenzofuran (PCDD to PCDF)

288 rom 6.8 years (1,2,3,7,8,9-hexachlorodibenzo-p-dioxin) to 11.6 years (pentachlorodibenzo-p-dioxin), w

289 l agonist of AhR (2,3,7,8-tetrachlorodibenzo-p-dioxin) to potentiate AhR transcriptional activity was

290 was reversed by 2,3,7, 8-tetrachlorodibenzo-p-dioxin treatment (TCDD).

291 for atrazine and 2,3,7,8-tetrachlorodibenzo-p-dioxin was 2.0 x 10(-10) M and 2.0 x 10(-11) M, respec

292 was formed from p-chlorophenol while dibenzo-p-dioxin was formed from o-chlorophenol.

293 otent AhR agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin was inactive.

294 d (2-azido-3-[(125)I]iodo-7,8-dibromodibenzo-p-dioxin), was assessed using both in vitro assays and a

295 receptor agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin whereas the equivalent wild-type EF cells expre

296 R ligands such as 2,3,7,8-tetrachlorodibenzo-p-dioxin, which has been attributed to the amino acid re

297 ntal contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin, which include the transcriptional activation o

298 when treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin, which induces this mRNA in wild-type Hepa-1 ce

299 ed higher reaction rate constants of dibenzo-p-dioxins with OH radicals than those of dibenzofurans.

300 -p-dioxin) to 11.6 years (pentachlorodibenzo-p-dioxin), with a composite half-life of 9.3 years for T