CORD-19:16a812de72963ceda960a168236e8dbe91832d45 / 18845-20039 JSONTXT

{"project":"CORD-19-SciBite-sentences","denotations":[{"id":"T193","span":{"begin":0,"end":1194},"obj":"http://purl.obolibrary.org/obo/HP0000707"},{"id":"T197","span":{"begin":0,"end":1194},"obj":"http://purl.obolibrary.org/obo/HP0011096"},{"id":"T199","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D017945"},{"id":"T201","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D014780"},{"id":"T205","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D051379"},{"id":"T208","span":{"begin":0,"end":1194},"obj":"http://purl.obolibrary.org/obo/GO0030424"},{"id":"T212","span":{"begin":0,"end":1194},"obj":"http://purl.obolibrary.org/obo/GO0008090"},{"id":"T213","span":{"begin":0,"end":1194},"obj":"http://purl.obolibrary.org/obo/GO0005883"},{"id":"T215","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D014777"},{"id":"T217","span":{"begin":0,"end":1194},"obj":"DX90170"},{"id":"T220","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D003711"},{"id":"T222","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D017945"},{"id":"T224","span":{"begin":0,"end":1194},"obj":"https://id.nlm.nih.gov/mesh/D009461"}],"attributes":[{"id":"A220","pred":"class","subj":"T220","obj":"INDICATION"},{"id":"A199","pred":"class","subj":"T199","obj":"SPECIES"},{"id":"A205","pred":"class","subj":"T205","obj":"SPECIES"},{"id":"A201","pred":"class","subj":"T201","obj":"SPECIES"},{"id":"A197","pred":"class","subj":"T197","obj":"HPO"},{"id":"A224","pred":"class","subj":"T224","obj":"INDICATION"},{"id":"A212","pred":"class","subj":"T212","obj":"GOONTOL"},{"id":"A217","pred":"class","subj":"T217","obj":"INDICATION"},{"id":"A193","pred":"class","subj":"T193","obj":"HPO"},{"id":"A215","pred":"class","subj":"T215","obj":"INDICATION"},{"id":"A222","pred":"class","subj":"T222","obj":"INDICATION"},{"id":"A213","pred":"class","subj":"T213","obj":"GOONTOL"},{"id":"A208","pred":"class","subj":"T208","obj":"GOONTOL"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}

{"project":"CORD-19_Custom_license_subset","denotations":[{"id":"T98","span":{"begin":0,"end":294},"obj":"Sentence"},{"id":"T99","span":{"begin":295,"end":592},"obj":"Sentence"},{"id":"T100","span":{"begin":593,"end":934},"obj":"Sentence"},{"id":"T101","span":{"begin":935,"end":1194},"obj":"Sentence"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}

{"project":"CORD-19-Sentences","denotations":[{"id":"TextSentencer_T98","span":{"begin":0,"end":294},"obj":"Sentence"},{"id":"TextSentencer_T99","span":{"begin":295,"end":592},"obj":"Sentence"},{"id":"TextSentencer_T100","span":{"begin":593,"end":934},"obj":"Sentence"},{"id":"TextSentencer_T101","span":{"begin":935,"end":1194},"obj":"Sentence"},{"id":"TextSentencer_T98","span":{"begin":0,"end":294},"obj":"Sentence"},{"id":"TextSentencer_T99","span":{"begin":295,"end":592},"obj":"Sentence"},{"id":"TextSentencer_T100","span":{"begin":593,"end":934},"obj":"Sentence"},{"id":"TextSentencer_T101","span":{"begin":935,"end":1194},"obj":"Sentence"},{"id":"T76450","span":{"begin":0,"end":294},"obj":"Sentence"},{"id":"T18711","span":{"begin":295,"end":592},"obj":"Sentence"},{"id":"T16835","span":{"begin":593,"end":934},"obj":"Sentence"},{"id":"T87816","span":{"begin":935,"end":1194},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}

{"project":"Epistemic_Statements","denotations":[{"id":"T45","span":{"begin":0,"end":294},"obj":"Epistemic_statement"},{"id":"T46","span":{"begin":935,"end":1194},"obj":"Epistemic_statement"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}

{"project":"CORD-19-PD-MONDO","denotations":[{"id":"T65","span":{"begin":51,"end":54},"obj":"Disease"},{"id":"T66","span":{"begin":770,"end":779},"obj":"Disease"},{"id":"T67","span":{"begin":843,"end":858},"obj":"Disease"},{"id":"T68","span":{"begin":849,"end":858},"obj":"Disease"},{"id":"T69","span":{"begin":900,"end":909},"obj":"Disease"},{"id":"T70","span":{"begin":1076,"end":1091},"obj":"Disease"},{"id":"T71","span":{"begin":1082,"end":1091},"obj":"Disease"}],"attributes":[{"id":"A65","pred":"mondo_id","subj":"T65","obj":"http://purl.obolibrary.org/obo/MONDO_0010518"},{"id":"A66","pred":"mondo_id","subj":"T66","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A67","pred":"mondo_id","subj":"T67","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A68","pred":"mondo_id","subj":"T68","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A69","pred":"mondo_id","subj":"T69","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"},{"id":"A70","pred":"mondo_id","subj":"T70","obj":"http://purl.obolibrary.org/obo/MONDO_0005108"},{"id":"A71","pred":"mondo_id","subj":"T71","obj":"http://purl.obolibrary.org/obo/MONDO_0005550"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}

{"project":"CORD-19-PD-HP","denotations":[{"id":"T49","span":{"begin":875,"end":888},"obj":"Phenotype"}],"attributes":[{"id":"A49","pred":"hp_id","subj":"T49","obj":"http://purl.obolibrary.org/obo/HP_0011096"}],"text":"However, we found that retrograde axonal transport was preserved in demyelinated mice with deletion of MHC class I (Ure and Rodriguez, 2002) , suggesting that the lack of CD8 + cytotoxic T-cells protected axonal integrity while not affecting demyelinated lesion load (Ure and Rodriguez, 2002) . A specific CD8+ T-cell-mediated response is further supported by our experiments showing that depletion of antigen-specific cytotoxic T-cells restricted to a viral peptide (VP2 121-130 ) resulted in preservation of neurological function, as measured by rotarod performance (Johnson et al., 2001) . Therefore, specific presentation of a Theiler's viral epitope within the context of H-2D b is necessary for at least a component of the neurological dysfunction associated with infection, although VP2 peptide depletion has no effect on the extent of viral infection or the level of demyelination induced by infection (Johnson et al., 2001) . Finally, ongoing experiments in our laboratory indicate that VP2 peptide depletion of the MHC class I cytotoxic T-cell response to Theiler's virus infection preserves spinal axons, as measured by neurofilament staining, axon counting, and retrograde labeling."}