ライフサイエンスコーパス: trinitrobenzene

1 l chemical inputs, namely chloride anion and trinitrobenzene.

2 with related nitroaromatic compounds (1,3,5 trinitrobenzene, 1,3 dinitrobenzene, and 2,4 dinitrotolu

3 ,4-dinitrotoluene, 1,3-dinitrobenzene, 1,3,5-trinitrobenzene, 2-amino-4,6-dinitrotoluene, 4-amino-2,6

4 says: TNT (4.3 +/- 2.6) x 10(8) M(-1); 1,3,5-trinitrobenzene (5.1 +/- 3.3) x 10(7) M(-1); picric acid

5 nd detection were selective for TNT and TNB (trinitrobenzene) but not RDX (hexahydro-1,3,5-trinitro-1

6 ene, 2,4-dinitrotoluene, 2,6-dinitrotoluene, trinitrobenzene, dinitrobenzene, or 1,3,5-trinitro-1,3,5

7 The substrate analog trinitrobenzene does not induce a substrate-like type I

8 ncentrations as low as parts per billion for trinitrobenzene, methylphosphonic acid, cysteine, and gl

9 ective in mucosal inflammation as modeled by trinitrobenzene sulfonate (TNBS) colitis.

10 ced in mice by intra-colonic instillation of Trinitrobenzene Sulfonate (TNBS).

11 administration of dextran sodium sulfate or trinitrobenzene sulfonate than mice with lower mucosal l

12 tran sodium sulfate or rectal application of trinitrobenzene sulfonate.

13 Trinitrobenzene sulfonic acid (TNBS) administration was

14 3p were tested in NCM460-NK-1R cells and the trinitrobenzene sulfonic acid (TNBS) and dextran sodium

15 s induced by dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) as well as nonstero

16 characterized by (i) loss of available 2,4,6-trinitrobenzene sulfonic acid (TNBS) binding to primary

17 itis and partially resistant to induction of trinitrobenzene sulfonic acid (TNBS) colitis and (2) mic

18 After induction of trinitrobenzene sulfonic acid (TNBS) colitis in SJL/J mi

19 The dextran sodium sulfate (DSS) and trinitrobenzene sulfonic acid (TNBS) colitis models were

20 necrosis factor-alpha (TNFalpha)] in murine trinitrobenzene sulfonic acid (TNBS) colitis, most likel

21 Chronic trinitrobenzene sulfonic acid (TNBS) colitis-associated

22 Mice administered intrarectal 2,4,6-trinitrobenzene sulfonic acid (TNBS) develop inflammatio

23 Colitis was induced via a 2.5% trinitrobenzene sulfonic acid (TNBS) enema.

24 ntal chronic colitis where administration of trinitrobenzene sulfonic acid (TNBS) in 50% ethanol indu

25 150 g-250 g) received 20 mg/rat intracolonic trinitrobenzene sulfonic acid (TNBS) in 50% ethanol or s

26 Colitis, induced by trinitrobenzene sulfonic acid (TNBS) in guinea pig, lead

27 y role in the T-cell helper 1 (Th1)-mediated trinitrobenzene sulfonic acid (TNBS) model of colitis.

28 age larvae, were given intrarectal saline or trinitrobenzene sulfonic acid (TNBS) on day 10 postinfec

29 n promoters; colitis was induced using 2,4,6-trinitrobenzene sulfonic acid (TNBS) or dextran sodium s

30 re compared to that found from the classical trinitrobenzene sulfonic acid (TNBS) procedure.

31 tes received dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) to induce intestina

32 In contrast, oral administration of trinitrobenzene sulfonic acid (TNBS) to Peyer's patch-nu

33 Foxo4-null mice were subjected to trinitrobenzene sulfonic acid (TNBS) treatment.

34 varia of 6-7-week-old mice administered with trinitrobenzene sulfonic acid (TNBS) with or without neu

35 Dextran sodium sulfate (DSS), 2,4,6-trinitrobenzene sulfonic acid (TNBS), and Salmonella typ

36 6 weeks posttransplantation by injection of trinitrobenzene sulfonic acid (TNBS), and tissues were a

37 f the Th1-mediated inflammation occurring in trinitrobenzene sulfonic acid (TNBS)-colitis.

38 e models of intestinal inflammation, we used trinitrobenzene sulfonic acid (TNBS)-hapten to induce in

39 of treating BALB/c mice with oxazolone- and trinitrobenzene sulfonic acid (TNBS)-induced colitides b

40 el disease and whether IL-16 participates in trinitrobenzene sulfonic acid (TNBS)-induced colitis in

41 Trinitrobenzene sulfonic acid (TNBS)-induced colitis in

42 Trinitrobenzene sulfonic acid (TNBS)-induced colitis is

43 ic regions associated with susceptibility to trinitrobenzene sulfonic acid (TNBS)-induced colitis wer

44 known about the effect of baicalein on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis, wh

45 FS1 in healthy and health-compromised, 2,4,6-trinitrobenzene sulfonic acid (TNBS)-treated mice.

46 s induced by the haptenating reagent, 2,4, 6-trinitrobenzene sulfonic acid (TNBS).

47 inistration of the haptenizing reagent 2,4,6-trinitrobenzene sulfonic acid (TNBS).

48 nduced by intracolonic instillation of 2,4,6-trinitrobenzene sulfonic acid (TNBS).

49 r dextran sulfate sodium salt (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS).

50 was induced using dextran sodium sulfate or trinitrobenzene sulfonic acid (TNBS).

51 uced by intracolonic administration of 2,4,6 trinitrobenzene sulfonic acid (TNBS).

52 shed by weekly intrarectal administration of trinitrobenzene sulfonic acid (TNBS).

53 tablished 6 days following administration of trinitrobenzene sulfonic acid (TNBS).

54 ter induction of ileitis by means of 2, 4, 6-trinitrobenzene sulfonic acid (TNBS)/ethanol installatio

55 following the intrarectal administration of trinitrobenzene sulfonic acid (TNBS-colitis), as well as

56 -mediated disease, the hapten reagent (2,4,6-trinitrobenzene sulfonic acid [TNBS])-induced colitis.

57 Using both the trinitrobenzene sulfonic acid and dextran sodium sulfate

58 fector phase exhibited a reduced severity of trinitrobenzene sulfonic acid colitis in association wit

59 These studies show that in chronic 2,4,6-trinitrobenzene sulfonic acid colitis, fibrosis is depen

60 T helper cell (Th)1-mediated inflammation in trinitrobenzene sulfonic acid colitis.

61 Six weekly 2,4,6-trinitrobenzene sulfonic acid enemas were given to estab

62 Female Lewis rats underwent weekly trinitrobenzene sulfonic acid enemas yielding models of

63 histologic scores, reduced serum anti-2,4,6-trinitrobenzene sulfonic acid IgG, decreased leukocyte i

64 Intracolonic administration of trinitrobenzene sulfonic acid in mice causes inflammatio

65 CP was induced by intraductal injection of trinitrobenzene sulfonic acid in rats.

66 In the murine trinitrobenzene sulfonic acid model of colitis, inhibiti

67 Colitis was induced with trinitrobenzene sulfonic acid or dextran sulfate sodium,

68 iven intrarectal hREG3A and exposed to 2,4,6-trinitrobenzene sulfonic acid showed less colon damage a

69 induced by dextran sulfate sodium (DSS) and trinitrobenzene sulfonic acid showed that TG FVB/6 mice

70 go spontaneous resolution, despite continued trinitrobenzene sulfonic acid stimulation.

71 11b(+) cells before colitis was induced with trinitrobenzene sulfonic acid to monitor the effects of

72 FVB/6 mice were more susceptible to DSS and trinitrobenzene sulfonic acid treatment than wild-type F

73 grity in tissues from distal colons of rats; trinitrobenzene sulfonic acid was used to induce inflamm

74 of PEG adducts by an indirect colorimetric (trinitrobenzene sulfonic acid) reaction, which detects l

75 ed 3 mouse models of IBD: colitis induced by trinitrobenzene sulfonic acid, colitis induced by microf

76 colonic inflammation after exposure to 2,4,6-trinitrobenzene sulfonic acid, compared with control mic

77 to membrane impermeable reagents, like 2,4,6-trinitrobenzene sulfonic acid, is also reduced severalfo

78 A membrane impermeant quencher, 2,4,6-trinitrobenzene sulfonic acid, or lipid-based quenchers

79 llenge in mice sensitized with hapten (2,4,6-trinitrobenzene sulfonic acid, TNBS).

80 ial regulation of ion transport in mice with trinitrobenzene sulfonic acid- or dextran sodium sulfate

81 elope prevented and treated a model of acute trinitrobenzene sulfonic acid-induced (TNBS-induced) col

82 ial function in vivo reduced the severity of trinitrobenzene sulfonic acid-induced colitis and associ

83 Anti-CD70 Ab treatment also suppressed trinitrobenzene sulfonic acid-induced colitis in SJL/J m

84 We studied this phenomenon in a chronic trinitrobenzene sulfonic acid-induced colitis model, an

85 In contrast, trinitrobenzene sulfonic acid-induced colitis, a predomi

86 y of tissue-specific PPAR-gamma null mice to trinitrobenzene sulfonic acid-induced colitis.

87 o protected against the development of 2,4,6-trinitrobenzene sulfonic acid-induced colitis.

88 significantly attenuated both DSS- and 2,4,6-trinitrobenzene sulfonic acid-induced colonic inflammati

89 erlying chronic inflammation and fibrosis in trinitrobenzene sulfonic acid-induced murine colitis.

90 , transfer (i.v.) of TGF-beta2-treated 2,4,6-trinitrobenzene sulfonic acid-pulsed bone marrow-derived

91 Mice that received 2,4,6-trinitrobenzene sulfonic acid-sensitized cells and chall

92 e the degree of digestion is determined with trinitrobenzene sulfonic acid.

93 /C mice after intracolonic administration of trinitrobenzene sulfonic acid.

94 awley rats by an intraductal injection of 2% trinitrobenzene sulfonic acid.

95 1-7 days after inflammation was induced with trinitrobenzene sulfonic acid.

96 uated colonic inflammatory pain induced with trinitrobenzene sulfonic acid.

97 igs and those treated 6 days previously with trinitrobenzene sulfonic acid.

98 4 T cells into rag2(-/-) recipients and (ii) trinitrobenzene sulfonic acid.

99 administration of dextran sodium sulfate or trinitrobenzene sulfonic acid.

100 ministered weekly doses of intrarectal 2,4,6-trinitrobenzene sulfonic acid.

101 induced in rats by intraductal injection of trinitrobenzene sulfonic acid.

102 navailable to chemical modification by 2,4,6-trinitrobenzene sulfonic acid.

103 nic insult by intraluminal administration of trinitrobenzene sulfonic acid; controls received saline.

104 trol and hREG3A-TG mice by administration of trinitrobenzene sulfonic acid; some mice were given intr

105 Colitis was induced in mice using trinitrobenzene sulfonic acid; symptoms were monitored a

106 ) mice by administration of ethanol; 2, 4, 6-trinitrobenzene sulfonic-acid (TNBS); or infection with

107 g) mice to induction of colitis with 2, 4, 6-trinitrobenzene-sulfonic-acid (TNBS), and the course of

108 olitis induced by dextran sulfate sodium and trinitrobenzene sulfuric acid, KO mice were more toleran

109 atients with inflamed colonic mucosa, and in trinitrobenzene sulphonic acid (TNBS) induced colitis in

110 We have previously demonstrated that trinitrobenzene sulphonic acid (TNBS)-induced colitis in

111 facilitation in the myenteric plexus of the trinitrobenzene sulphonic acid-inflamed guinea-pig dista

112 nzene (TCTNB), 1:1 DADP/1,3,5-tribromo-2,4,6-trinitrobenzene (TBTNB), and 1:1 DADP/1,3,5-triiodo-2,4,

113 e explosives: 1:1 DADP/1,3,5-trichloro-2,4,6-trinitrobenzene (TCTNB), 1:1 DADP/1,3,5-tribromo-2,4,6-t

114 ne (TBTNB), and 1:1 DADP/1,3,5-triiodo-2,4,6-trinitrobenzene (TITNB).

115 g an Affi-Gel resin derivatized with a 2,4,6-trinitrobenzene (TNB) moiety and a fluorophore-labeled a

116 ol (TNP), 2,4,6-trinitrotoluene (TNT), 1,3,5-trinitrobenzene (TNB), and 2,4-dinitrotoluene (DNT).

117 sives, 2,4,6-trinitrotoluene (TNT) and 1,3,5-trinitrobenzene (TNB), are often encountered together as

118 Upon exposure to trinitrobenzene (TNB), the self-assembled structures for

119 Concentrations of 1 ppm of trinitrobenzene (TNB), trinitrotoluene (TNT), dinitroben

120 of a soluble analyte, fluorescently labeled trinitrobenzene, to surface-immobilized monoclonal anti-

121 rotoluenes, dinitrobenzene, trinitrotoluene, trinitrobenzene, two aminodinitrotoluenes, three nitroes

122 1-Cyano-2,4,6-trinitrobenzene was found to be the most reactive and th