{'fraction_non_alphanumeric': 0.026166097838452786, 'fraction_numerical': 0.006825938566552901, 'mean_word_length': 5.027397260273973, '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}}
Action of epsilon-aminocaproic acid on the proteolysis system during experimental influenza in mice.

Proteolysis system was examined in influenza-virus-infected mice after a 5-day course of therapeutic or preventive treatments with the proteolysis inhibitor epsilon-aminocaproic acid (E-ACA). The mice were infected with nonadapted influenza virus A/Hong Kong/1/68 (H3N2). E-ACA was shown to exert a pathogenetic action expressed by a marked tendency to normalization of elevated alkaline protease activity in damaged lung tissue and in the blood of infected animals. E-ACA induced a long-lasting high level activity of acidic proteases in the blood which correlated with increased protection of animals against influenza virus infection. It may be suggested that acidic proteases are involved in the preventive action of E-ACA and are a factor of resistance to virus infection.