{'fraction_non_alphanumeric': 0.018229166666666668, 'fraction_numerical': 0.0026041666666666665, 'mean_word_length': 5.6869565217391305, '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}}
CIRCULATING ANTIBODY FOLLOWING CARDIAC TRANSPLANTATION IN Ag‐B‐COMPATIBLE RATS1

Lymphocytotoxio antibody was consistently present in the serum of untreated rat recipients bearing Ag-B-compatible heterotopic cardiac transplants. In most cases antibody appeared within 5 days, which was before the first signs of endothelial damage in the graft arteries. High antibody levels were present in the serum of a recipient bearing a long-term, strongly beating transplant. Increasing doses of azathioprine inhibited or prevented antibody formation. The findings suggest that initial damage to the endothelial cells of rat cardiac graft vessels is caused by circulating antibody. Subsequent development of arterial intimal thickening appears to have a cell-mediated component.