{'fraction_non_alphanumeric': 0.03333333333333333, 'fraction_numerical': 0.0031746031746031746, 'mean_word_length': 5.31, '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}}
Pathogenesis of experimental endolymphatic hydrops.

The protein content and the d.c. potential of the endolymph differs in the various parts of the endolymphatic space (cochlea, utricle, semicircular canals and endolymphatic sac) as also does the ion composition (chloride, potassium, sodium). 12 months after obliteration of the endolymphatic sac and duct in guinea pigs the d.c. potential falls, whereas, the sodium activity increases. The endolymphatic hydrops is not caused by an increased colloid osmotic pressure. The increased water-binding capacity of the cochlear endolymph is correlated with the increased Na+ activity.