Id |
Subject |
Object |
Predicate |
Lexical cue |
T209 |
0-10 |
Sentence |
denotes |
Discussion |
T11625 |
11-246 |
Sentence |
denotes |
The major findings in the present study are that TNF-α signaling showed cellular specific responses of NF-κB phosphorylation in the PC following SE, which may be related to vasogenic edema formation followed by neutrophil infiltration. |
T210 |
11-246 |
Sentence |
denotes |
The major findings in the present study are that TNF-α signaling showed cellular specific responses of NF-κB phosphorylation in the PC following SE, which may be related to vasogenic edema formation followed by neutrophil infiltration. |
T11626 |
247-332 |
Sentence |
denotes |
BBB disruption has been reported in experimental and human epilepsy [12,13,15,16,28]. |
T211 |
247-332 |
Sentence |
denotes |
BBB disruption has been reported in experimental and human epilepsy [12,13,15,16,28]. |
T11627 |
333-470 |
Sentence |
denotes |
Leakage of serum-derived components into the extracellular space is associated with hyperexcitability and seizure onset [12,13,15,16,28]. |
T212 |
333-470 |
Sentence |
denotes |
Leakage of serum-derived components into the extracellular space is associated with hyperexcitability and seizure onset [12,13,15,16,28]. |
T11628 |
471-592 |
Sentence |
denotes |
Furthermore, dysfunction of the BBB leads to epileptogenesis and contributes to progression of epilepsy [12,13,15,16,28]. |
T213 |
471-592 |
Sentence |
denotes |
Furthermore, dysfunction of the BBB leads to epileptogenesis and contributes to progression of epilepsy [12,13,15,16,28]. |
T11629 |
593-697 |
Sentence |
denotes |
In the present study, TNF-α immunoreactivity was obviously observed in microglia in the PC following SE. |
T214 |
593-697 |
Sentence |
denotes |
In the present study, TNF-α immunoreactivity was obviously observed in microglia in the PC following SE. |
T11630 |
698-814 |
Sentence |
denotes |
TNF receptor expressions were also up-regulated in astrocytes (TNFp55R and TNFp75R) and endothelial cells (TNFp75R). |
T215 |
698-814 |
Sentence |
denotes |
TNF receptor expressions were also up-regulated in astrocytes (TNFp55R and TNFp75R) and endothelial cells (TNFp75R). |
T11631 |
815-985 |
Sentence |
denotes |
Furthermore, blockade of TNF-α signaling by sTNFp55 infusion effectively (but not completely) reduced volumes of SE-induced vasogenic edema and neuronal damage in the PC. |
T216 |
815-985 |
Sentence |
denotes |
Furthermore, blockade of TNF-α signaling by sTNFp55 infusion effectively (but not completely) reduced volumes of SE-induced vasogenic edema and neuronal damage in the PC. |
T11632 |
986-1149 |
Sentence |
denotes |
These findings indicate that TNF-α may participate in astroglial and endothelial responses to SE, which are relevant to SE-induced vasogenic edema formation [5-8]. |
T217 |
986-1149 |
Sentence |
denotes |
These findings indicate that TNF-α may participate in astroglial and endothelial responses to SE, which are relevant to SE-induced vasogenic edema formation [5-8]. |
T11633 |
1150-1245 |
Sentence |
denotes |
Indeed, TNF-α signaling increases BBB permeability in various experimental disease models [29]. |
T218 |
1150-1245 |
Sentence |
denotes |
Indeed, TNF-α signaling increases BBB permeability in various experimental disease models [29]. |
T11634 |
1246-1371 |
Sentence |
denotes |
In the present study, sTNFp55 infusion could not completely prevent SE-induced vasogenic edema and neuronal damage in the PC. |
T219 |
1246-1371 |
Sentence |
denotes |
In the present study, sTNFp55 infusion could not completely prevent SE-induced vasogenic edema and neuronal damage in the PC. |
T11635 |
1372-1491 |
Sentence |
denotes |
Therefore, our findings suggest that TNF-α signaling may not be a unique upstream event in vasogenic edema development. |
T220 |
1372-1491 |
Sentence |
denotes |
Therefore, our findings suggest that TNF-α signaling may not be a unique upstream event in vasogenic edema development. |
T11636 |
1492-1636 |
Sentence |
denotes |
p65 phosphorylation of NF-κB enhances its transactivation potential, and p65 phosphorylation occurs in either the cytoplasm or the nucleus [30]. |
T221 |
1492-1636 |
Sentence |
denotes |
p65 phosphorylation of NF-κB enhances its transactivation potential, and p65 phosphorylation occurs in either the cytoplasm or the nucleus [30]. |
T11637 |
1637-1812 |
Sentence |
denotes |
In the present study, p65-Thr435 immunoreactivity was detected in endothelial cells, and its immunoreactivity showed an inverse correlation to the degree of SMI-71 expression. |
T222 |
1637-1812 |
Sentence |
denotes |
In the present study, p65-Thr435 immunoreactivity was detected in endothelial cells, and its immunoreactivity showed an inverse correlation to the degree of SMI-71 expression. |
T11638 |
1813-1913 |
Sentence |
denotes |
SMI-71, an endothelial barrier antigen, is a protein expressed by endothelial cells of rat BBB [31]. |
T223 |
1813-1913 |
Sentence |
denotes |
SMI-71, an endothelial barrier antigen, is a protein expressed by endothelial cells of rat BBB [31]. |
T11639 |
1914-2006 |
Sentence |
denotes |
Under pathological conditions, SMI-71 expression is lost in endothelial cells [5,7,8,30,32]. |
T224 |
1914-2006 |
Sentence |
denotes |
Under pathological conditions, SMI-71 expression is lost in endothelial cells [5,7,8,30,32]. |
T11640 |
2007-2135 |
Sentence |
denotes |
Acute phases of the above pathological conditions are accompanied by opening of the BBB and development of vasogenic edema [33]. |
T225 |
2007-2135 |
Sentence |
denotes |
Acute phases of the above pathological conditions are accompanied by opening of the BBB and development of vasogenic edema [33]. |
T11641 |
2136-2375 |
Sentence |
denotes |
Indeed, neutralization of SMI-71 in vivo leads to widening of intercellular junctions between endothelial cells and swelling of perivascular astrocytic processes [34], although SMI-71 is not localized at endothelial cell junctions [35-38]. |
T226 |
2136-2375 |
Sentence |
denotes |
Indeed, neutralization of SMI-71 in vivo leads to widening of intercellular junctions between endothelial cells and swelling of perivascular astrocytic processes [34], although SMI-71 is not localized at endothelial cell junctions [35-38]. |
T11642 |
2376-2535 |
Sentence |
denotes |
In the present study, SMI-71 immunoreactivity was significantly reduced in blood vessels 1 day after SE when vasogenic edema and neuronal damage were observed. |
T227 |
2376-2535 |
Sentence |
denotes |
In the present study, SMI-71 immunoreactivity was significantly reduced in blood vessels 1 day after SE when vasogenic edema and neuronal damage were observed. |
T11643 |
2536-2623 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively prevented SE-induced SMI-71 down-regulation. |
T228 |
2536-2623 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively prevented SE-induced SMI-71 down-regulation. |
T11644 |
2624-2924 |
Sentence |
denotes |
With respect to the phosphorylation of p65-Thr435 by TNF-α [39], our findings indicate that TNF-α-mediated p65-Thr435 phosphorylation in endothelial cells may play an important role in vasogenic edema induction via SMI-71 degradation or its posttranslational dysfunction influencing BBB permeability. |
T229 |
2624-2924 |
Sentence |
denotes |
With respect to the phosphorylation of p65-Thr435 by TNF-α [39], our findings indicate that TNF-α-mediated p65-Thr435 phosphorylation in endothelial cells may play an important role in vasogenic edema induction via SMI-71 degradation or its posttranslational dysfunction influencing BBB permeability. |
T11645 |
2925-3216 |
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 |
2925-3216 |
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 |
3217-3380 |
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 |
3217-3380 |
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 |
3381-3510 |
Sentence |
denotes |
In the present study, p65-Ser276, p65-Ser311, p65-Ser529, and p65-Ser536 phosphorylation was observed in astrocytes following SE. |
T232 |
3381-3510 |
Sentence |
denotes |
In the present study, p65-Ser276, p65-Ser311, p65-Ser529, and p65-Ser536 phosphorylation was observed in astrocytes following SE. |
T11648 |
3511-3632 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively inhibited p65-Ser276 and p65-Ser311phosphorylation in astrocytes following SE. |
T233 |
3511-3632 |
Sentence |
denotes |
Furthermore, sTNFp55R infusion effectively inhibited p65-Ser276 and p65-Ser311phosphorylation in astrocytes following SE. |
T11649 |
3633-3762 |
Sentence |
denotes |
Therefore, it is likely that enhanced p65-Ser276 and p65-Ser311 phosphorylation may be involved in TNF-α-mediated BBB disruption. |
T234 |
3633-3762 |
Sentence |
denotes |
Therefore, it is likely that enhanced p65-Ser276 and p65-Ser311 phosphorylation may be involved in TNF-α-mediated BBB disruption. |
T11650 |
3763-3867 |
Sentence |
denotes |
However, sTNFp55R infusion could not prevent p65-Ser529 and p65-Ser536 phosphorylations from SE insults. |
T235 |
3763-3867 |
Sentence |
denotes |
However, sTNFp55R infusion could not prevent p65-Ser529 and p65-Ser536 phosphorylations from SE insults. |
T11651 |
3868-4062 |
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 |
3868-4062 |
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 |
4063-4259 |
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 |
4063-4259 |
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. |
T11653 |
4260-4411 |
Sentence |
denotes |
Neutrophil infiltration into brain parenchyma is transiently observed during the acute phase of SE (4 - 36 hr after SE) and disappears thereafter [20]. |
T238 |
4260-4411 |
Sentence |
denotes |
Neutrophil infiltration into brain parenchyma is transiently observed during the acute phase of SE (4 - 36 hr after SE) and disappears thereafter [20]. |
T11654 |
4412-4511 |
Sentence |
denotes |
SE rapidly increases synthesis and release of chemokines in various areas of the rodent brain [42]. |
T239 |
4412-4511 |
Sentence |
denotes |
SE rapidly increases synthesis and release of chemokines in various areas of the rodent brain [42]. |
T11655 |
4512-4618 |
Sentence |
denotes |
Among them, MIP-2 is required for efficient neutrophil or lymphocyte recruitment to brain parenchyma [43]. |
T240 |
4512-4618 |
Sentence |
denotes |
Among them, MIP-2 is required for efficient neutrophil or lymphocyte recruitment to brain parenchyma [43]. |
T11656 |
4619-4757 |
Sentence |
denotes |
In our previous study [20], neutrophil infiltration in the frontoparietal cortex was regulated by P2X7 receptor-mediated MIP-2 expression. |
T241 |
4619-4757 |
Sentence |
denotes |
In our previous study [20], neutrophil infiltration in the frontoparietal cortex was regulated by P2X7 receptor-mediated MIP-2 expression. |
T11657 |
4758-4903 |
Sentence |
denotes |
In the PC, however, neither a P2X7 receptor agonist/antagonist nor IL-1Ra (an IL-1β antagonist) infusion could not affect leukocyte infiltration. |
T242 |
4758-4903 |
Sentence |
denotes |
In the PC, however, neither a P2X7 receptor agonist/antagonist nor IL-1Ra (an IL-1β antagonist) infusion could not affect leukocyte infiltration. |
T11658 |
4904-5068 |
Sentence |
denotes |
In the present study, sTNFp55R infusion effectively inhibited neutrophil infiltration in the PC by reducing vasogenic edema formation in a MIP-2-independent manner. |
T243 |
4904-5068 |
Sentence |
denotes |
In the present study, sTNFp55R infusion effectively inhibited neutrophil infiltration in the PC by reducing vasogenic edema formation in a MIP-2-independent manner. |
T11659 |
5069-5308 |
Sentence |
denotes |
With respect to the present and our previous reports, it is therefore likely that vasogenic edema induced by TNF-α can induce neutrophil infiltration and press injury to evoke neuronal-astroglial loss in the PC, unlike other brain regions. |
T244 |
5069-5308 |
Sentence |
denotes |
With respect to the present and our previous reports, it is therefore likely that vasogenic edema induced by TNF-α can induce neutrophil infiltration and press injury to evoke neuronal-astroglial loss in the PC, unlike other brain regions. |
T11660 |
5309-5564 |
Sentence |
denotes |
In conclusion, our findings reveal that impairments of endothelial cell function via TNF-α mediated p65-Thr 435 NF-κB phosphorylation may be involved in SE-induced vasogenic edema, which is relevant to neutrophil infiltration and neuronal-astroglial loss. |
T245 |
5309-5564 |
Sentence |
denotes |
In conclusion, our findings reveal that impairments of endothelial cell function via TNF-α mediated p65-Thr 435 NF-κB phosphorylation may be involved in SE-induced vasogenic edema, which is relevant to neutrophil infiltration and neuronal-astroglial loss. |