{'fraction_non_alphanumeric': 0.02528735632183908, 'fraction_numerical': 0.00996168582375479, 'mean_word_length': 5.248803827751196, '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}}
[Hydrogen metabolism in the large intestine--physiology and clinical implications].

During the anaerobic metabolism of the colonic bacterial flora short chain fatty acids and the gases hydrogen (H2) and carbon dioxyde (CO2) are produced. In about 50% of a European and North-American population and in 90% of rural black Africans, methane is generated from H2 and CO2. In methane-negative individuals, sulfate reducing bacteria utilize H2 to reduce sulfate to sulfide. Methanogenesis and sulfate reduction are usually mutually exclusive. A competition exists for the common substrate hydrogen which is potentially regulated by the availability of sulfate in the colonic lumen. Other bacteria can use H2 to reduce CO2 to acetate (homoacetogenesis). Methane is an inert gas and has probably no direct effect in man. The metabolites of sulfate reduction (mercaptides, hydrogen sulfide) are toxic and hydrogen sulfide is supposed to play a role in the pathogenesis of ulcerative colitis. All H2-utilizing metabolisms reduce the gaseous volume in the colon and thus prevent flatulence. In patients with pneumatosis cystoides intestinalis methanogenesis is absent and sulfate reduction is insignificant. This deficiency provides an explanation for the massive H2-excretion in those patients and their symptoms.