{'fraction_non_alphanumeric': 0.03282828282828283, 'fraction_numerical': 0.023989898989898988, 'mean_word_length': 5.244094488188976, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 1, '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}}
Factor XI gene analysis in thrombophilia and factor XI deficiency

(or <0.9) associated with carriage of the G allele, and an odds ratio >1.3 (or <0.8) associated with homozygosity for the G allele (P 1⁄4 0.05). These results lead us to conclude that the FccRIIa G507A polymorphism does not contribute to risk of MI in the population examined, either alone or in combination with established cardiovascular risk factors. Our findings support those of an earlier study [12], which demonstrated differential binding of activation-dependent antibodies by platelets that was dependent on the FccRIIa G507A polymorphism, but which also failed to demonstrate genotype-dependent differences in intrinsic platelet function as assessed by agonist and shear-induced platelet activation and aggregation.