CORD-19:16a812de72963ceda960a168236e8dbe91832d45 / 452-709
Annnotations
CORD-19_Custom_license_subset
{"project":"CORD-19_Custom_license_subset","denotations":[{"id":"T6","span":{"begin":33,"end":171},"obj":"Sentence"}],"text":"ock (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). However, clinical and basic science observations have begun to challenge this hypothe"}
CORD-19-Sentences
{"project":"CORD-19-Sentences","denotations":[{"id":"TextSentencer_T6","span":{"begin":33,"end":171},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":33,"end":171},"obj":"Sentence"},{"id":"T35322","span":{"begin":33,"end":171},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"ock (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). However, clinical and basic science observations have begun to challenge this hypothe"}
CORD-19-PD-MONDO
{"project":"CORD-19-PD-MONDO","denotations":[{"id":"T2","span":{"begin":147,"end":165},"obj":"Disease"},{"id":"T3","span":{"begin":167,"end":169},"obj":"Disease"}],"attributes":[{"id":"A2","pred":"mondo_id","subj":"T2","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"http://purl.obolibrary.org/obo/MONDO_0005301"}],"text":"ock (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). However, clinical and basic science observations have begun to challenge this hypothe"}
CORD-19-PD-HP
{"project":"CORD-19-PD-HP","denotations":[{"id":"T4","span":{"begin":110,"end":123},"obj":"Phenotype"}],"attributes":[{"id":"A4","pred":"hp_id","subj":"T4","obj":"http://purl.obolibrary.org/obo/HP_0011096"}],"text":"ock (McDonald and Sears, 1969) . Such observations appeared sufficient to explain the majority of deficits in demyelinating human diseases such as multiple sclerosis (MS). However, clinical and basic science observations have begun to challenge this hypothe"}