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 tochemically to form polychlorinated dibenzo-p-dioxins.

17 racterized toxicants polychlorinated dibenzo-p-dioxins.

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

19 (2,3,7,8-TeCDD), 1,2,3,4-tetrachlorodibenzo-p-dioxin (1,2,3,4-TeCDD), and 2,7-dichlorodibenzo-p-diox

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

21 1-, 2-MCDD), 1,6-, 1,9-, 1,3-dichlorodibenzo-p-dioxin (1,6-, 1,9-, 1,3-DCDD), 4-monochlorodibenzofura

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

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

24 y experiment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (2,3,7,8-TeCDD), 1,2,3,4-tetrachlorodibenzo-p-d

25 xin (1,2,3,4-TeCDD), and 2,7-dichlorodibenzo-p-dioxin (2,7-DiCDD) as target organohalides.

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

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

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

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

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

31 r, a new data set of polychlorinated dibenzo-p-dioxin and dibenzofuran (PCDD/Fs) half-lives (HLs) in

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

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

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

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

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

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

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

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

40 ,7,8-Br-substituted tri- to octabromodibenzo-p-dioxins and -furans, and all 210 polychlorinated diben

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 ed biphenyls (PCBs), polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs), and polybrominated diben

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

66 furans (PCDD/Fs), and polybrominated dibenzo-p-dioxins and furans, with THs [total (L)-thyroxine (TT(

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

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

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

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

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

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

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

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

75 wo representative PCDDs, 2,3-dichlorodibenzo-p-dioxin (BCDD) and 2,3,7,8-tetrachlorodibenzo-p-dioxin

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

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

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

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

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

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

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

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

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

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

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

87 tion of two classes of photoproducts-dibenzo-p-dioxins (DDs) and 2,2'-dihydroxylated biphenyls-was al

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 Polychlorinated dibenzo-p-dioxins (PCDDs) are a class of toxic organic compounds

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

137 Polychlorinated dibenzo-p-dioxins (PCDDs), as a class of persistent and highly t

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

139 The levels of polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated dibenzofurans (PCDFs)

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and other aryl hydrocarbon receptor (AhR

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

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

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

162 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related halogenated aromatic hydroca

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

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

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

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

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

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

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

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

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

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

173 ally gavaged with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) every 4 days for 28 days.

174 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exhibits antiestrogenic properties, incl

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

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

177 ted the impact of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure, a ubiquitous and highly toxic

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

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

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

181 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) impairs craniofacial skeletal developmen

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

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

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

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

216 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a prototypical Ahr agonist, had an indu

217 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a widespread environmental contaminant,

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

219 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), an aryl hydrocarbon receptor (AhR) agon

220 The compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, is a pote

221 manifestations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant, primarily

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

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

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

225 dioxin (BCDD) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), based on the fluorescence quenching.

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

227 proteins bind to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), but stronger binding to gmAhr1a was obs

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

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

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

231 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), for which the epidemiological evidence

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

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

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

235 tor (AHR) ligand, 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), induces CYP1 family enzymes, which can

236 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is primarily produced via industrial pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

252 ontaminant called 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

280 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD, or dioxin) is known to induce rapid infl

281 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD; dioxin) is a toxic environmental contami

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

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

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

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

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

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

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

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

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

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

292 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

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

294 ng direct photolysis and 2,8-dichlorodibenzo-p-dioxin was only found during direct photolysis at pH 8

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

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