{'fraction_non_alphanumeric': 0.020257826887661142, 'fraction_numerical': 0.0, 'mean_word_length': 6.4520547945205475, '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}}
Levels of antibodies against cytomegalovirus and Chlamydophila pneumoniae are increased in early onset pre‐eclampsia

Objective The origins of pre‐eclampsia/eclampsia lie in a mismatch between feto‐placental demands and utero‐placental supply, a situation that also arises in normotensive intrauterine growth restriction (IUGR). Could reactivated chronic infection be both a trigger for these differential maternal responses to the same underlying pathology and a link between pre‐eclampsia and its attendant lifelong risks of atherosclerosis?