PMC:7565665 / 20842-21165
Annnotations
LitCovid-PD-FMA-UBERON
| Id | Subject | Object | Predicate | Lexical cue | fma_id |
|---|---|---|---|---|---|
| T113 | 133-141 | Body_part | denotes | alveolar | http://purl.org/sig/ont/fma/fma264783 |
LitCovid-PD-MONDO
| Id | Subject | Object | Predicate | Lexical cue | mondo_id |
|---|---|---|---|---|---|
| T157 | 188-198 | Disease | denotes | infections | http://purl.obolibrary.org/obo/MONDO_0005550 |
| T158 | 281-301 | Disease | denotes | respiratory diseases | http://purl.obolibrary.org/obo/MONDO_0005087 |
LitCovid-PD-CLO
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T231 | 0-1 | http://purl.obolibrary.org/obo/CLO_0001020 | denotes | A |
LitCovid-PubTator
| Id | Subject | Object | Predicate | Lexical cue | tao:has_database_id |
|---|---|---|---|---|---|
| 526 | 188-198 | Disease | denotes | infections | MESH:D007239 |
| 527 | 281-301 | Disease | denotes | respiratory diseases | MESH:D012140 |
LitCovid-PD-HP
| Id | Subject | Object | Predicate | Lexical cue | hp_id |
|---|---|---|---|---|---|
| T61 | 115-131 | Phenotype | denotes | oxidative stress | http://purl.obolibrary.org/obo/HP_0025464 |
| T62 | 178-198 | Phenotype | denotes | recurrent infections | http://purl.obolibrary.org/obo/HP_0002719 |
LitCovid-PD-GO-BP
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T295 | 43-52 | http://purl.obolibrary.org/obo/GO_0016236 | denotes | autophagy |
| T296 | 43-52 | http://purl.obolibrary.org/obo/GO_0006914 | denotes | autophagy |
| T297 | 142-151 | http://purl.obolibrary.org/obo/GO_0097194 | denotes | apoptosis |
| T298 | 142-151 | http://purl.obolibrary.org/obo/GO_0006915 | denotes | apoptosis |
| T299 | 153-172 | http://purl.obolibrary.org/obo/GO_0090398 | denotes | cellular senescence |
| T300 | 231-243 | http://purl.obolibrary.org/obo/GO_0009405 | denotes | pathogenesis |
LitCovid-sentences
| Id | Subject | Object | Predicate | Lexical cue |
|---|---|---|---|---|
| T112 | 0-323 | Sentence | denotes | A number of recent studies have identified autophagy dysfunction as the central mechanism of elevated inflammatory-oxidative stress, alveolar apoptosis, cellular senescence, and recurrent infections, all of which contribute to the pathogenesis and progression of acute and chronic respiratory diseases [22,35,61,62,70,111]. |