| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-96 |
Sentence |
denotes |
Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice. |
| TextSentencer_T2 |
97-287 |
Sentence |
denotes |
Accumulating 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. |
| TextSentencer_T3 |
288-572 |
Sentence |
denotes |
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). |
| TextSentencer_T4 |
573-732 |
Sentence |
denotes |
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. |
| TextSentencer_T5 |
733-987 |
Sentence |
denotes |
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 < 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. |
| TextSentencer_T6 |
988-1162 |
Sentence |
denotes |
Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. |
| TextSentencer_T7 |
1163-1412 |
Sentence |
denotes |
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. |
| TextSentencer_T8 |
1413-1584 |
Sentence |
denotes |
Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 > apoE3 = apoE2) in genetically engineered mice. |
| T1 |
0-96 |
Sentence |
denotes |
Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in mice. |
| T2 |
97-287 |
Sentence |
denotes |
Accumulating 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. |
| T3 |
288-572 |
Sentence |
denotes |
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). |
| T4 |
573-732 |
Sentence |
denotes |
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. |
| T5 |
733-987 |
Sentence |
denotes |
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 < 0.001 for each comparison), with no significant differences between 2/2 and 3/3 KI mice. |
| T6 |
988-1162 |
Sentence |
denotes |
Immunohistochemistry for human apoE expression revealed similar apoE distribution with no significant difference in the immunostaining intensity among the 3 lines of KI mice. |
| T7 |
1163-1412 |
Sentence |
denotes |
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. |
| T8 |
1413-1584 |
Sentence |
denotes |
Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 > apoE3 = apoE2) in genetically engineered mice. |
