{'fraction_non_alphanumeric': 0.010964912280701754, 'fraction_numerical': 0.0021929824561403508, 'mean_word_length': 5.308755760368664, '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}}
DELAYED REMYELINATION IN RAT SPINAL CORD FOLLOWING ETHIDIUM BROMIDE INJECTION

Areas of demyelination were produced by injecting ethidium bromide into the white matter of the lumbar spinal cord of rats. There was variation in the nature of the process of demyelination and a difference in the speed with which Schwann cells remyelinated the demyelinated axons. In some lesions, or areas within lesions, myelin debris was rapidly processed by macrophages and axons were rapidly remyelinated by Schwann cells, while in other lesions of similar duration, or in areas within the same lesion, the myelin was transformed into lattices of membranous profiles which persisted around axons for long periods of time. In the lesions containing such myelin derived membranes, there were few macrophages and remyelination by Schwann cells was delayed compared to that seen in the more rapidly resolving lesions. It was concluded that the slow resolution of some lesions resulted from the delay between intoxication and cell disintegration (7–10 days) which meant that the cell responses to demyelination took place in a glial free area which could not support cell movement needed for removal of myelin debris and remyelination. This study indicates that the tempo and results of demyelination can be altered by the cellular events which accompany degeneration of oligodendrocytes.