ライフサイエンスコーパス: hepatotoxin

1 nd reduced liver damage in mice exposed to a hepatotoxin.

2 ethionine has been identified as a potential hepatotoxin.

3 and cholestasis, when exposed to nine known hepatotoxins.

4 though some had exposures to other potential hepatotoxins.

5 iver-specific products and susceptibility to hepatotoxins.

6 ng hepatotoxic injury by alcohol and various hepatotoxins.

7 ought to light a few new agents as potential hepatotoxins.

8 event in liver necrosis caused by alkylating hepatotoxins.

9 athology in response to ischemia and certain hepatotoxins.

10 vels found in the liver after treatment with hepatotoxins.

11 ittermates were challenged by feeding with a hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine (D

12 human FL-HCC, as well as treatment with the hepatotoxin 3,5-diethoxycarbonyl-1,4-dihydrocollidine, w

13 g administration of the metabolism-dependent hepatotoxin acetaminophen (APAP) or the direct nephrotox

14 lso enhance sensitivity to the albumin-bound hepatotoxin, acetaminophen (APAP).

15 t Fxralpha-/- mice, after treatment with the hepatotoxin alpha-naphthylisothiocyanate, which is known

16 Aflatoxin B1 (AFB1) is a human hepatotoxin and hepatocarcinogen produced by the mold As

17 for patients with NAFLD include avoidance of hepatotoxins and aggressive management of associated con

18 tochrome P450 2E1 (CYP2E1) activates several hepatotoxins and contributes to alcoholic liver damage.

19 be important in CYP2E1-catalyzed toxicity of hepatotoxins and in alcohol-induced liver injury.

20 Since hepatotoxins are associated with increased keratin phosp

21 ynthesis of cylindrospermopsin (1), a potent hepatotoxin associated with the cyanobacterium Cylindros

22 Another 7 (2%) were direct hepatotoxins but only in high doses and placed in a sepa

23 ntrols before and after a single dose of the hepatotoxin carbon tetrachloride and hybridized them aga

24 12 weeks by intraperitoneal injection of the hepatotoxin carbon tetrachloride.

25 after chronic injury inflicted by iterative hepatotoxin (carbon tetrachloride) injection and bile du

26 l animals following exposure to the chemical hepatotoxin, carbon tetrachloride (CCl4).

27 The hepatotoxin CCl(4) induced activation of RSK, phosphoryl

28 pressed inflammatory responses in a model of hepatotoxin (CCl4 )-induced hepatitis, but surprisingly

29 rious conditions, including systemic injury, hepatotoxin exposure, and warm ischemia.

30 charide (LPS) alone or LPS together with the hepatotoxin galactosamine (GalN) was performed to identi

31 ver, exposure of S52A-expressing mice to the hepatotoxins, griseofulvin or microcystin, which are ass

32 This microcystin analog and potent hepatotoxin has previously been known only from the aqua

33 of urine following administration of a model hepatotoxin hydrazine.

34 strate that the production of cyanobacterial hepatotoxins in lichen symbiosis is a global phenomenon

35 to COL1 were more resistant to a variety of hepatotoxins, in a dose-dependent manner, and had lower

36 several new reports of previously recognized hepatotoxins, including herbal products, were published.

37 aling provides hepatocyte protection against hepatotoxin-induced apoptosis.

38 ytokine but is hepatoprotective in models of hepatotoxin-induced liver fibrosis.

39 revents T/NKT cell hepatitis but exacerbates hepatotoxin-induced liver injury by inhibiting macrophag

40 lished prednisolone-mediated exacerbation of hepatotoxin-induced liver injury.

41 oxl1-expressing cells are not the origin for hepatotoxin-induced liver tumors.

42 neages during liver injury in the context of hepatotoxin-inhibited hepatocyte proliferation.

43 data identify FKB as a potent GSH-sensitive hepatotoxin, levels of which should be specifically moni

44 found that, after fibrotic liver injury from hepatotoxins, LSECs become highly proinflammatory and se

45 tecting all the 11 tested commonly occurring hepatotoxins (MC-LR, -dmlR, -RR, -dmRR, -LA, -LY, -LF, -

46 alpha-galactosylceramide (alpha-GalCer), and hepatotoxin-mediated hepatitis induced by carbon tetrach

47 e display library against the cyanobacterial hepatotoxin microcystin LR and its selection using compe

48 of cyclic peptides, including the widespread hepatotoxins microcystins and nodularins.

49 Among well described hepatotoxins, new reports appeared with highly active an

50 that copper may be acting in synergy with a hepatotoxin, or 2) that there may be a genetic predispos

51 xification and subsequent elimination of the hepatotoxin, over AFB1 exo-8,9-oxidation.

52 The hepatotoxin phomopsin A (PHO-A), a secondary metabolite

53 The transport of microcystin, a hepatotoxin produced by cyanobacteria (e.g., Microcystis

54 Microcystins (MCs) are primarily hepatotoxins produced by cyanobacteria and are responsib

55 Microcystins (MCs) are hepatotoxins produced by cyanobacteria responsible for t

56 Microcystins (MCs) are a group of hepatotoxins produced by cyanobacteria that have not had

57 stins, the highly toxic low-molecular-weight hepatotoxins produced by cyanobacteria.

58 nd INH causes accumulation of the endogenous hepatotoxin protoporphyrin IX in the liver through PXR-m

59 er regeneration, inflammatory bowel disease, hepatotoxin sensitivity, and the diagnostic, persistent

60 against cholestatic liver injury induced by hepatotoxin such as ANIT.

61 ls has been shown to occur after exposure to hepatotoxins such as CCl4.

62 nmentally exposed to cyanobacteria producing hepatotoxins, such as microcystins (MCs), together with

63 and for the hepatocyte apoptosis induced by hepatotoxins that results in liver injury.

64 trasubstituted piperidine A-ring unit of the hepatotoxin was efficiently constructed.

65 astically increased and toxicity of a set of hepatotoxins was detected at clinically relevant concent

66 ter bromobenzene (BB), a model GSH-depleting hepatotoxin, was administered to the Syrian hamster.