Id |
Subject |
Object |
Predicate |
Lexical cue |
T1 |
0-152 |
Sentence |
denotes |
Nitrogen Mustard-Induced Corneal Injury Involves DNA Damage and Pathways Related to Inflammation, Epithelial-Stromal Separation, and Neovascularization. |
T1 |
0-152 |
Sentence |
denotes |
Nitrogen Mustard-Induced Corneal Injury Involves DNA Damage and Pathways Related to Inflammation, Epithelial-Stromal Separation, and Neovascularization. |
T2 |
153-161 |
Sentence |
denotes |
PURPOSE: |
T2 |
153-161 |
Sentence |
denotes |
PURPOSE: |
T3 |
162-370 |
Sentence |
denotes |
To evaluate the toxic effects and associated mechanisms in corneal tissue exposed to the vesicating agent, nitrogen mustard (NM), a bifunctional alkylating analog of the chemical warfare agent sulfur mustard. |
T3 |
162-370 |
Sentence |
denotes |
To evaluate the toxic effects and associated mechanisms in corneal tissue exposed to the vesicating agent, nitrogen mustard (NM), a bifunctional alkylating analog of the chemical warfare agent sulfur mustard. |
T4 |
371-379 |
Sentence |
denotes |
METHODS: |
T4 |
371-379 |
Sentence |
denotes |
METHODS: |
T5 |
380-549 |
Sentence |
denotes |
Toxic effects and associated mechanisms were examined in maximally affected corneal tissue using corneal cultures and human corneal epithelial (HCE) cells exposed to NM. |
T5 |
380-549 |
Sentence |
denotes |
Toxic effects and associated mechanisms were examined in maximally affected corneal tissue using corneal cultures and human corneal epithelial (HCE) cells exposed to NM. |
T6 |
550-558 |
Sentence |
denotes |
RESULTS: |
T6 |
550-558 |
Sentence |
denotes |
RESULTS: |
T7 |
559-802 |
Sentence |
denotes |
Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. |
T7 |
559-802 |
Sentence |
denotes |
Analysis of ex vivo rabbit corneas showed that NM exposure increased apoptotic cell death, epithelial thickness, epithelial-stromal separation, and levels of vascular endothelial growth factor, cyclooxygenase 2, and matrix metalloproteinase-9. |
T8 |
803-1014 |
Sentence |
denotes |
In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. |
T8 |
803-1014 |
Sentence |
denotes |
In HCE cells, NM exposure resulted in a dose-dependent decrease in cell viability and proliferation, which was associated with DNA damage in terms of an increase in p53 ser15, total p53, and H2A.X ser139 levels. |
T9 |
1015-1185 |
Sentence |
denotes |
NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. |
T9 |
1015-1185 |
Sentence |
denotes |
NM exposure also induced caspase-3 and poly ADP ribose polymerase cleavage, suggesting their involvement in NM-induced apoptotic death in the rabbit cornea and HCE cells. |
T10 |
1186-1500 |
Sentence |
denotes |
Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. |
T10 |
1186-1500 |
Sentence |
denotes |
Similar to rabbit cornea, NM exposure caused an increase in cyclooxygenase 2, matrix metalloproteinase-9, and vascular endothelial growth factor levels in HCE cells, indicating a role of these molecules and related pathways in NM-induced corneal inflammation, epithelial-stromal separation, and neovascularization. |
T11 |
1501-1771 |
Sentence |
denotes |
NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury. |
T11 |
1501-1771 |
Sentence |
denotes |
NM exposure also induced activation of activator protein 1 transcription factor proteins and upstream signaling pathways including mitogen-activated protein kinases and Akt protein kinase, suggesting that these could be key factors involved in NM-induced corneal injury. |
T12 |
1772-1784 |
Sentence |
denotes |
CONCLUSIONS: |
T12 |
1772-1784 |
Sentence |
denotes |
CONCLUSIONS: |
T13 |
1785-2086 |
Sentence |
denotes |
Results from this study provide insight into the molecular targets and pathways that could be involved in NM-induced corneal injuries laying the background for further investigation of these pathways in vesicant-induced ocular injuries, which could be helpful in the development of targeted therapies. |
T13 |
1785-2086 |
Sentence |
denotes |
Results from this study provide insight into the molecular targets and pathways that could be involved in NM-induced corneal injuries laying the background for further investigation of these pathways in vesicant-induced ocular injuries, which could be helpful in the development of targeted therapies. |