{'fraction_non_alphanumeric': 0.01780821917808219, 'fraction_numerical': 0.00410958904109589, 'mean_word_length': 6.092233009708738, '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}}
Ultrastructural and Immunofluorescent Studies of Acute and Chronic Lactate Dehydrogenase Elevating Virus-Induced Nonparalytic Poliomyelitis in Mice

Abstract Light microscopic, electron microscopic, and immunofluorescent studies have been performed on young C58/J mice following administration of cyclophosphamide and peripheral inoculation of the C strain of lactate dehydrogenase-elevating virus (LDV-C). Using special fixation techniques, all three types of studies were performed on the spinal cord tissues obtained from the same mice. LDV-C infection-specific immunofluorescence was detected in anterior horn neurons. Ultrastructurally, anterior horn neurons during the acute inflammatory phase of the disease were characterized by various degrees of chromatolysis, an increase in the number of lamellar inclusion bodies, and extensive membrane proliferation of perinuclear endocytoplasmic reticulum. A chronic vacuolar appearance of the anterior horn was due to intraneuronal vacuolation as well as vacuolation of the neuropil; these changes may have been due to expansion of proliferated intracytoplasmic membranes and/or focal ischemia secondary to the acute inflammatory response. Direct evidence was obtained that indicated the cytopathology was not immune mediated in that highly poliomyelitis-susceptible 18-month-old C58/J mice developed severe paralysis without inflammation of the spinal cord when treated with cyclophosphamide before infection.