{'fraction_non_alphanumeric': 0.012432012432012432, 'fraction_numerical': 0.0, 'mean_word_length': 5.887700534759358, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Histological and histometric examination of the intrahepatic portal vein branches in primary biliary cirrhosis without regenerative nodules.

Histometric examination, based on the assumption that ratios of the sizes of portal vein branches to the sizes of the accompanying hepatic arterial branches in the portal tracts are relatively constant in normal livers, indicated that in primary biliary cirrhosis without regenerative nodules, lumens of the intrahepatic portal veins were narrowed and phlebosclerosis was frequent in patients with esophageal varices. Thus, each of these lesions of the intrahepatic portal veins might be related to the development of the presinusoidal portal hypertension that occurs in primary biliary cirrhosis without regenerative nodules. However, the exact causal relationship of this portal venopathy and the development of portal hypertension remains unknown. Damage to the intrahepatic bile ducts in primary biliary cirrhosis, associated with portal and periportal inflammation, may contribute to the development of the morphological lesions of the intrahepatic portal veins. Furthermore, spongiomatous vasculatures found around the larger portal veins, but not those around the smaller veins, appear to be related to the presence of esophageal varices.