ライフサイエンスコーパス: hepatotoxic

1 old lower vector dose was significantly less hepatotoxic.

2 However, statins can be hepatotoxic.

3 e FMOs metabolites seem to be neurotoxic and hepatotoxic.

4 nd the alternative--propylthiouracil--can be hepatotoxic.

5 a commonly used analgesic, it can be highly hepatotoxic.

6 mulation in the liver, and excessive iron is hepatotoxic.

7 ins free nicotinic acid, but some brands are hepatotoxic.

8 be one of the mechanisms by which ethanol is hepatotoxic.

9 stinal, two allergic); three late syndromes (hepatotoxic, accelerated nephrotoxic, erythromelalgia);

10 inds and inactivates the highly reactive and hepatotoxic acetaminophen metabolite N-acetyl-p-benzoqui

11 Hepatotoxic aflatoxins have found a worthy adversary in

12 ly promotes liver damage and is not a direct hepatotoxic agent.

13 mal manifestations require the withdrawal of hepatotoxic agents and the reversal of hepatic iron over

14 Chronic exposure of the liver to hepatotoxic agents initiates an aberrant wound healing r

15 A number of other hepatotoxic agents, such as d-galactosamine, CCl4, and t

16 here it is known to potentiate the action of hepatotoxic agents.

17 fects of acetaminophen and potentially other hepatotoxic agents.

18 l-para-aminophenol (APAP, or paracetamol), a hepatotoxic analgesic drug.

19 y bile acid lithocholic acid (LCA), which is hepatotoxic and a potential enteric carcinogen.

20 Beyond normal therapeutic doses, the drug is hepatotoxic and genotoxic.

21 agonist of the nuclear receptor FXR was not hepatotoxic and had no regulatory effects.

22 mouse liver following administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that

23 derivative lithocholic acid (LCA) is highly hepatotoxic and, as we show here, a metabolic substrate

24 MCs are hepatotoxic, and acute exposure causes severe liver dama

25 ial for apoptosis-inducing activity of a non-hepatotoxic anti-Fas mAb HFE7A.

26 ged liver microenvironment was not, however, hepatotoxic, because CBLB502 induced resistance to Fas-m

27 -dose UDCA could result in the production of hepatotoxic bile acids, such as lithocholic acid (LCA),

28 holestasis to diminish uptake of potentially hepatotoxic bile acids.

29 result from the joint effects of viruses and hepatotoxic chemical carcinogens.

30 nonimmunologically by chronic exposure to a hepatotoxic chemical.

31 ary epithelial cells are targets for certain hepatotoxic chemicals, including some procarcinogens, th

32 as MeOH-2, and MeOH-3, completely devoid of hepatotoxic components.

33 re we show that treatment with two different hepatotoxic compounds (acetaminophen and thioacetamide)

34 l genomic prediction technique for screening hepatotoxic compounds based on in vitro human liver cell

35 ning technique that can identify potentially hepatotoxic compounds in the early stages of drug develo

36 is B virus infection and dietary exposure to hepatotoxic contaminants.

37 ystems and influences liver repair following hepatotoxic damage or regeneration following partial hep

38 Administration of a hepatotoxic diet containing 0.1% 3,5-diethoxycarbonyl-1,

39 .4 mg/mL, 8 microL/h) 4 to 16 hours before a hepatotoxic dose of acetaminophen (600 mg/kg, intraperit

40 lowing administration of non-hepatotoxic and hepatotoxic doses in vivo, implying that Nrf2 may have a

41 Hepatotoxic doses of acetaminophen to mice produce not o

42 in rats and several patients after consuming hepatotoxic doses of APAP.

43 liver injury, rats were treated either with hepatotoxic doses of D-(+)-galactosamine (DGAL) or aceta

44 TNF-alpha before administration of low, but hepatotoxic, doses of CCl4.

45 ed hepatocellular disease by administering a hepatotoxic drug and compared the hepatic extraction eff

46 ate production caused by the addition of the hepatotoxic drug Bosentan was determined.

47 Dogs that were affected by the hepatotoxic drug had reduced HEE.

48 s progression of liver injury even after the hepatotoxic drug is cleared from the body.

49 toxicity analysis was performed for fifteen hepatotoxic drugs by evaluating toxic changes reflecting

50 applied to clinical case studies to identify hepatotoxic drugs in complex comedication regimes to fur

51 Failure to predict hepatotoxic drugs in preclinical testing makes it impera

52 The risk associated with exposure to hepatotoxic drugs is difficult to quantify.

53 Acute liver failure induced by hepatotoxic drugs results from rapid progression of inju

54 ule-of-two positives, 14 were withdrawn from hepatotoxic drugs, and one was over-the-counter medicati

55 ld-type mice when co-administered with known hepatotoxic drugs.

56 T observed in some patients suggested a mild hepatotoxic effect of IFN.

57 cycloheximide, thus suggesting the indirect hepatotoxic effect of MIP2.

58 while chronic exposure produces only a rare hepatotoxic effect.

59 P, which c) elicited maternal thyrotoxic and hepatotoxic effects and d) induced MNGs in the fetal tes

60 Perfluorooctanoic acid (PFOA or C8) has hepatotoxic effects in animals.

61 The long-term implications of hepatotoxic effects in patients with psoriasis remains u

62 Hepatotoxic effects of APAP-mediated Ca2+ deregulation w

63 re, postulated that DC may also modulate the hepatotoxic effects of APAP.

64 nce of the livers may have resulted from the hepatotoxic effects of chemotherapy and/or hepatic infil

65 Liver injury is thought to be caused by the hepatotoxic effects of the retained alpha1-ATZ.

66 GstP null mice were highly resistant to the hepatotoxic effects of this compound.

67 und to be considerably less sensitive to its hepatotoxic effects than wild-type animals, indicating t

68 , monitor for the development of MTX-induced hepatotoxic effects, and monitor for worsening of hepati

69 abortifacient despite its potentially lethal hepatotoxic effects.

70 ot provide any indication that FIAU would be hepatotoxic in humans.

71 first time in detail, may contribute to the hepatotoxic, inflammatory, and tumorigenic action of MC-

72 stress, reactive oxygen species, and causing hepatotoxic injury by alcohol and various hepatotoxins.

73 Oral administration of VLX103 also decreased hepatotoxic injury in a second more chronic model of alc

74 that liver regeneration induced by an acute hepatotoxic injury promotes expansion of transplanted he

75 According to this model, hepatotoxic insults select for hepatocytes with specific

76 has been reported to protect against various hepatotoxic insults, influences the susceptibility of mi

77 estingly, Gadd45beta ablation did not affect hepatotoxic JNK signaling after a TNFR-mediated immune c

78 this drug in the prevention and treatment of hepatotoxic liver injury.

79 Thus, rather than being hepatotoxic, liver triglyceride accumulation is actually

80 ranscript knockdown in mice treated with non-hepatotoxic LNA ASOs, while the levels of many unintende

81 ranscripts were reduced in mice treated with hepatotoxic LNA ASOs.

82 nel of highly efficacious hepatotoxic or non-hepatotoxic LNA ASOs.

83 We examined hepatotoxic mechanisms in mice homozygous for the severe

84 as issues surrounding the use of potentially hepatotoxic medications in patients with underlying chro

85 With respect to using potentially hepatotoxic medications in patients with underlying live

86 Finally, the use of potentially hepatotoxic medications in patients with underlying live

87 The use of potentially hepatotoxic medications in patients with underlying live

88 included: history of hepatitis, exposure to hepatotoxic medications, prior weight loss surgery, and

89 cause of insufficient liver tissue or use of hepatotoxic medications, so 148 remained in the study (m

90 tabolic conversion of the drug to its active hepatotoxic metabolite.

91 -, and CYP3A4-driven conversion of APAP into hepatotoxic metabolites.

92 For example, members of a few genera produce hepatotoxic microcystins, whereas production of hepatoto

93 Using cholestatic and hepatotoxic models of liver injury, we compared the deve

94 In various hepatotoxic models, both pro- and anti-inflammatory acti

95 asing the expression and accumulation of the hepatotoxic mutant protein.

96 atotoxic microcystins, whereas production of hepatotoxic nodularins appears to be limited to a single

97 e treated with a panel of highly efficacious hepatotoxic or non-hepatotoxic LNA ASOs.

98 but also differences in the intake of other hepatotoxic or protective factors, differences in the ce

99 -treated Era(-/-) mice developed none of the hepatotoxic phenotypes such as hepatomegaly, elevation i

100 The hepatotoxic potential of 3-hydroxy-3-methylglutaryl coen

101 tive ability of HCV-specific T cells and the hepatotoxic potential that they possess, there is a grea

102 s a more direct and mechanistic indicator of hepatotoxic potential.

103 okine milieu drive both hepatoprotective and hepatotoxic processes.

104 and 0.15% of those completing treatment) had hepatotoxic reactions to isoniazid during preventive tre

105 and investigated the potential mechanisms of hepatotoxic sensitivity.

106 tifs (TCC and TGC) that were present only in hepatotoxic sequences.

107 Tolcapone is also known for its hepatotoxic side effects even though it is therapeutical

108 t graft-protective attributes and the lowest hepatotoxic side effects.

109 e was demonstrated to be a safe drug without hepatotoxic side effects.

110 ny older agents, in some cases expanding the hepatotoxic spectrum for the drugs.

111 In mice, different hepatotoxic stimuli linked with the development of diffe

112 dose >50 mg (n = 50) were significantly more hepatotoxic than compounds belonging to other groups.

113 drate-derived palmitate in the liver is more hepatotoxic than dietary palmitate.

114 However, only one of them was less hepatotoxic than tacrine in HepG2 cells.

115 lipids and their metabolites are potentially hepatotoxic, the absence of overt injury in fatty livers

116 patitis viruses appear to be synergistically hepatotoxic; this synergy appears to explain both the hi

117 These data strongly suggest that hepatotoxic TRO causes apoptosis by activating the JNK-d

118 ydroxylation, leading to the accumulation of hepatotoxic unsaturated monohydroxy bile acids.

119 elicits metabolic perturbations that may be hepatotoxic, we investigated the relationship between fr