These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Apoptosis and cell proliferation in biliary atresia.
    Author: Funaki N, Sasano H, Shizawa S, Nio M, Iwami D, Ohi R, Nagura H.
    Journal: J Pathol; 1998 Dec; 186(4):429-33. PubMed ID: 10209494.
    Abstract:
    Biliary atresia (BA), which is thought to result from progressive destruction of the bile ducts by a necroinflammatory process, is the most common cause of obstructive jaundice in infancy. Abnormalities in the cell turnover of remodelling ductal plates are considered one of the important aetiological factors in this disorder, but little work has been done on this topic. Programmed cell death or apoptosis was therefore examined by TdT-mediated dUTP biotin nick end labelling (TUNEL) and cell proliferation by Ki67 immunostaining in 34 cases of BA. The results were compared with normal control liver (five cases) and congenital dilatation of the bile ducts (CDB, five cases) in order to study the cell turnover or tissue dynamics of BA. The TUNEL labelling index (LI) in bile ducts (48.9 +/- 13.2 per cent) was significantly higher than that of the control normal liver (3.6 +/- 2.8 per cent) and of CDB (2.5 +/- 5.1 per cent). The Ki67 LI in the bile ducts of BA (15.0 +/- 5.57 per cent) was also significantly higher than that of CDB (8.6 +/- 5.4 per cent). No significant differences of the TUNEL and Ki67 LIs in hepatocytes were, however, observed between BA, CDB, and normal liver. The TUNEL LI was significantly higher than the Ki67 LI in the bile ducts of BA. BA is therefore associated with increased and disorganized cell turnover of the bile ducts, which is related to malformation of the ductal plate or abnormal bile duct development.
    [Abstract] [Full Text] [Related] [New Search]