Id |
Subject |
Object |
Predicate |
Lexical cue |
T11645 |
0-291 |
Sentence |
denotes |
In our previous studies [5,8], dystrophin (an actin-binding protein [40]) immunoreactivity was detected in blood vessels and in astrocytic perivascular end-feet, and was down-regulated 12 hrs after SE prior to the appearance of vasogenic edema and down-regulation of SMI-71 immunoreactivity. |
T230 |
0-291 |
Sentence |
denotes |
In our previous studies [5,8], dystrophin (an actin-binding protein [40]) immunoreactivity was detected in blood vessels and in astrocytic perivascular end-feet, and was down-regulated 12 hrs after SE prior to the appearance of vasogenic edema and down-regulation of SMI-71 immunoreactivity. |
T11646 |
292-455 |
Sentence |
denotes |
With respect to this previous report, changes in SMI immunoreactivity would be causes/results of interaction between endothelial cells and perivascular astrocytes. |
T231 |
292-455 |
Sentence |
denotes |
With respect to this previous report, changes in SMI immunoreactivity would be causes/results of interaction between endothelial cells and perivascular astrocytes. |
T11647 |
456-585 |
Sentence |
denotes |
In the present study, p65-Ser276, p65-Ser311, p65-Ser529, and p65-Ser536 phosphorylation was observed in astrocytes following SE. |
T232 |
456-585 |
Sentence |
denotes |
In the present study, p65-Ser276, p65-Ser311, p65-Ser529, and p65-Ser536 phosphorylation was observed in astrocytes following SE. |
T11648 |
586-707 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively inhibited p65-Ser276 and p65-Ser311phosphorylation in astrocytes following SE. |
T233 |
586-707 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively inhibited p65-Ser276 and p65-Ser311phosphorylation in astrocytes following SE. |
T11649 |
708-837 |
Sentence |
denotes |
Therefore, it is likely that enhanced p65-Ser276 and p65-Ser311 phosphorylation may be involved in TNF-α-mediated BBB disruption. |
T234 |
708-837 |
Sentence |
denotes |
Therefore, it is likely that enhanced p65-Ser276 and p65-Ser311 phosphorylation may be involved in TNF-α-mediated BBB disruption. |
T11650 |
838-942 |
Sentence |
denotes |
However, sTNFp55R infusion could not prevent p65-Ser529 and p65-Ser536 phosphorylations from SE insults. |
T235 |
838-942 |
Sentence |
denotes |
However, sTNFp55R infusion could not prevent p65-Ser529 and p65-Ser536 phosphorylations from SE insults. |
T11651 |
943-1137 |
Sentence |
denotes |
Since p65-Ser529 and p65-Ser536 are phosphorylated by TNF-α and IL-1β [41], it is likely that IL-1β-mediated p65-Ser529/Ser536 phosphorylation may also play a role in SE-induced vasogenic edema. |
T236 |
943-1137 |
Sentence |
denotes |
Since p65-Ser529 and p65-Ser536 are phosphorylated by TNF-α and IL-1β [41], it is likely that IL-1β-mediated p65-Ser529/Ser536 phosphorylation may also play a role in SE-induced vasogenic edema. |
T11652 |
1138-1334 |
Sentence |
denotes |
Therefore, our findings indicate that both TNF-α and IL-1β may be synergists to play either a direct (by endothelial cells) or indirect (by astrocytes) role in the maintenance of BBB permeability. |
T237 |
1138-1334 |
Sentence |
denotes |
Therefore, our findings indicate that both TNF-α and IL-1β may be synergists to play either a direct (by endothelial cells) or indirect (by astrocytes) role in the maintenance of BBB permeability. |