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[Fatal fulminating hepatitis induced by nilutamide]
[Article in French]
Edouard A, Robinel R, Rat C, Lombard F, Lorinet C, Escarmant P.
Publication Types:
PMID: 14770126 [PubMed - indexed for MEDLINE]
-
[Gabapentine-induced acute hepatitis]
[Article in French]
Bureau C, Poirson H, Peron JM, Vinel JP.
Publication Types:
PMID: 14770125 [PubMed - indexed for MEDLINE]
-
[Acute hepatitis due to Exolise, a Camellia sinensis-derived drug]
[Article in French]
Vial T, Bernard G, Lewden B, Dumortier J, Descotes J.
Publication Types:
PMID: 14770123 [PubMed - indexed for MEDLINE]
-
[Etifoxine chlorhydrate-induced acute hepatitis]
[Article in French]
Mennecier D, Rimlinger H, Gidenne S, Moulin O, Marzars H, Thiolet C, Farret O.
Publication Types:
PMID: 14732859 [PubMed - indexed for MEDLINE]
-
Use of propofol for alcohol withdrawal delirium: a case report.
Takeshita J.
Publication Types:
PMID: 14974494 [PubMed - indexed for MEDLINE]
A dog bite to the eyelid.
Imran D, Mandal A.
Department of Plastic Surgery, Norfolk and Norwich University Hospital, UK. surgeonimran@yahoo.co.uk
Publication Types:
PMID: 14749404 [PubMed - indexed for MEDLINE]
Comment on:
Enterobacter sakazakii--new foods for thought?
Farber JM.
Bureau of Microbial Hazards, A.L. 2203G3, Food Directorate, Health Canada, Ottawa, K1A 0L2, Ontario, Canada. Jeff_Farber@hc-sc.gc.ca
Publication Types:
PMID: 14723984 [PubMed - indexed for MEDLINE]
Endothelial cell injury and coagulation system activation during synergistic hepatotoxicity from monocrotaline and bacterial lipopolysaccharide coexposure.
Yee SB, Hanumegowda UM, Copple BL, Shibuya M, Ganey PE, Roth RA.
Department of Pharmacology, National Food Safety and Toxicology Center, Institute for Environmental Toxicology, Michigan State University, East Lansing, USA.
A small, noninjurious dose of bacterial lipopolysaccharide (LPS; 7.4 x 106 EU/kg) administered 4 h after a small, nontoxic dose of monocrotaline (MCT; 100 mg/kg) produces synergistic hepatotoxicity in rats within 6 to 12 h after MCT exposure. The resulting centrilobular (CL) and midzonal (MZ) liver lesions are characterized by hepatic parenchymal cell (HPC) necrosis. Pronounced hemorrhage, disruption of sinusoidal architecture, and loss of central vein intima suggest that an additional component to injury may be the liver vasculature. In the present investigation, the hypothesis that sinusoidal endothelial cell (SEC) injury and coagulation system activation occur in this model was tested. Plasma hyaluronic acid (HA) concentration, a biomarker for SEC injury, was significantly increased in cotreated animals before the onset of HPC injury and remained elevated through the time of maximal HPC injury (i.e., 18 h). SEC injury was confirmed by immunohistochemistry and electron microscopy. Pyrrolic metabolites were produced from MCT by SECs in vitro, which suggests that MCT may injure SECs directly through the formation of its toxic metabolite, monocrotaline pyrrole. Inasmuch as SEC activation and injury can promote hemostasis, activation of the coagulation system was evaluated. Coagulation system activation, as marked by a decrease in plasma fibrinogen, occurred before the onset of HPC injury. Furthermore, extensive fibrin deposition was observed immunohistochemically within CL and MZ regions after MCT/LPS cotreatment. Taken together, these results suggest that SEC injury and coagulation system activation are components of the synergistic liver injury resulting from MCT and LPS coexposure.
PMID: 12730616 [PubMed - indexed for MEDLINE]
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