{'fraction_non_alphanumeric': 0.022479564032697547, 'fraction_numerical': 0.006811989100817439, 'mean_word_length': 5.5874439461883405, '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}}
DIFFERENTIAL SUSCEPTIBILITY OF CARDIAC CELL POPULATIONS TO IN VITRO IMMUNE INJURY

In vitro, the culture of enzymatically dissociated fetal heart cells results in the formation of contractile cellular islets surrounded by monolayers of static cells. The islets contract in a spontaneous and synchronous fashion. Using inbred strains of rats sensitized by an allogeneic heart transplant or by three consecutive skin grafts, immune sera were obtained that were assayed at various dilutions against the cell cultures with or without complement. Strain-specific and selective lysis exclusively directed against the static cells was observed. This suggests that noncontractile cells were the specific targets for alloantibody in this fetal heart cell culture system. Clinical, as well as experimental, rejection of transplanted organs correlates histologically with the disruption of normal parenchymal architecture by local inflammation and destruction (1–3). Afferent and efferent mechanisms of rejection have been described with various organ components acting as either sensitizing agents or as targets, such as passenger leukocytes (4, 5), endothelial cells (6, 7), basement membranes (3), or organ-specific parenchymal cells (9, 10). To study the targets of rat allograft rejection in vitro, we have developed a tissue culture assay to look at the degree of damage of parenchymal contractile heart cells and other static cardiac cells when exposed to alloimmune sera.