{'fraction_non_alphanumeric': 0.02072192513368984, 'fraction_numerical': 0.0006684491978609625, 'mean_word_length': 5.0120481927710845, '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}}
Variations in albumin use in patients with cirrhosis: An AASLD members survey

serum iron was already maximal at the basal state and was not significantly affected by the high-iron diet. Wu et al. likewise investigated the responses of the mutant mice to iron. The mice were previously placed on an iron-deficient diet (immediately after weaning) to prevent excessive iron accumulation and subsequently subjected to acute iron challenge by oral gavage. This manipulation increases serum iron without affecting hepatic iron stores; thus, hepcidin induction is driven exclusively by serum iron. Under these conditions, Hjv and HfeHjv mice failed to mount any hepcidin response, contrary to wild-type and Hfe controls. The authors concluded that Hjv and Hfe play distinct roles in regulating hepcidin.1 However, this interpretation does not take into account the key finding that coelimination of Hfe did not exacerbate the phenotype of Hjv deficiency. Hemochromatosis is not acute but develops over time due to unrestricted dietary iron absorption. The experimental iron-loading approaches undertaken by Wu et al. and Kent et al. are diverse but complementary, and all results are consistent with earlier work showing that hepcidin responds to hepatic and serum iron by distinct mechanisms. Moreover, they validate previous data with single Hfe and Hjv mice, showing that Hfe and Hjv are both dispensable for hepatic iron sensing, while only Hjv, but not Hfe, is required for sensing of serum iron.