PubMed:12638732 JSONTXT

{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":97,"end":287},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":288,"end":572},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":573,"end":732},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":733,"end":987},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":988,"end":1162},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":1163,"end":1412},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":1413,"end":1584},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":96},"obj":"Sentence"},{"id":"T2","span":{"begin":97,"end":287},"obj":"Sentence"},{"id":"T3","span":{"begin":288,"end":572},"obj":"Sentence"},{"id":"T4","span":{"begin":573,"end":732},"obj":"Sentence"},{"id":"T5","span":{"begin":733,"end":987},"obj":"Sentence"},{"id":"T6","span":{"begin":988,"end":1162},"obj":"Sentence"},{"id":"T7","span":{"begin":1163,"end":1412},"obj":"Sentence"},{"id":"T8","span":{"begin":1413,"end":1584},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":673,"end":690},"obj":"HP_0002637"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"12638732-3#46#51#gene348","span":{"begin":619,"end":624},"obj":"gene348"},{"id":"12638732-3#100#117#diseaseC0007785","span":{"begin":673,"end":690},"obj":"diseaseC0007785"},{"id":"12638732-3#100#117#diseaseC0917798","span":{"begin":673,"end":690},"obj":"diseaseC0917798"}],"relations":[{"id":"46#51#gene348100#117#diseaseC0007785","pred":"associated_with","subj":"12638732-3#46#51#gene348","obj":"12638732-3#100#117#diseaseC0007785"},{"id":"46#51#gene348100#117#diseaseC0917798","pred":"associated_with","subj":"12638732-3#46#51#gene348","obj":"12638732-3#100#117#diseaseC0917798"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T2502","span":{"begin":619,"end":624},"obj":"gene:348"},{"id":"T2503","span":{"begin":673,"end":690},"obj":"disease:C0007785"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2502","obj":"T2503"},{"id":"R2","pred":"associated_with","subj":"T2502","obj":"T2503"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":42,"end":47},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":252,"end":257},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":387,"end":392},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":759,"end":764},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1485,"end":1490},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":718,"end":724},"obj":"http://purl.obolibrary.org/obo/UBERON_4200215"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":42,"end":47},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":252,"end":257},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":387,"end":392},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":759,"end":764},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":1485,"end":1490},"obj":"http://purl.obolibrary.org/obo/UBERON_0000955"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":718,"end":724},"obj":"http://purl.obolibrary.org/obo/UBERON_4200215"},{"id":"PD-UBERON-AE-B_T7","span":{"begin":1223,"end":1230},"obj":"http://purl.obolibrary.org/obo/UBERON_2000602"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":1202,"end":1206},"obj":"gene:348"},{"id":"T1","span":{"begin":1403,"end":1411},"obj":"disease:C0022116"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice.\nAccumulating evidence suggests that among the 3 human apolipoprotein E (apoE) isoforms encoded by the human APOE gene, the e4 allele may act to exacerbate brain damage in humans and animals. This study aimed to compare the isoform-specific vulnerability conferred by human apoE to ischemic brain damage, using mice expressing human apoE isoforms (apoE2, apoE3, or apoE4) in place of mouse apoE, produced by the gene-targeting technique in embryonic stem cells (knock-in, KI). Homozygous human apoE2 (2/2), apoE3 (3/3), or apoE4 (4/4) KI mice were subjected to permanent focal cerebral ischemia by a modified intraluminal suture method. Twenty-four h thereafter, brain damage, (as estimated by infarct volume and neurologic deficit) was significantly worse in 4/4 KI mice versus 2/2 or 3/3 KI mice (p \u003c 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. Notably. increased expression of human apoE was detected in neurons and astrocytes in the peri-infarct area, and a punctate expression pattern was evident in the border between the infarct and peri-infarct areas in all KI mice subjected to ischemia. Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 \u003e apoE3 = apoE2) in genetically engineered mice."}