PMC:2800179 / 17711-20327 JSON TXT

Annnotations TAB JSON ListView MergeView

GO-CC

{"project":"GO-CC","denotations":[{"id":"T8047","span":{"begin":484,"end":489},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T8048","span":{"begin":857,"end":862},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T8049","span":{"begin":1112,"end":1117},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T8050","span":{"begin":1379,"end":1384},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T8051","span":{"begin":1446,"end":1451},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T8052","span":{"begin":1629,"end":1634},"obj":"http://purl.obolibrary.org/obo/GO_0005623"},{"id":"T16272","span":{"begin":1928,"end":1933},"obj":"http://purl.obolibrary.org/obo/GO_0005623"}],"text":"Degraded CGN Induced-TNF-α Production by Monocytes In Vitro \nIn order to study the capacity of dCGN to stimulate TNF-α production, peripheral blood monocytes were cultivated in the presence of dCGN (0.1 to 1 mg/ml). Very low levels of TNF-α were induced in PBM after stimulation with native CGN (Fig. 2A). Addition of 0.1 mg/ml 10 kDa dCGN resulted in approximately a 60-fold increase in TNF-α production by PBM. This was a dose-dependent effect that reached a 180-fold increase when cells were exposed to 1 mg/ml of 10 kDa dCGN (Fig. 2A). A 250-fold increase in TNF-α production was detected at 1 mg/ml 40 kDa dCGN (Fig. 2A). TNF-α production increased in time reaching a maximum level at 8 hours of culture (Figure 2B). After 24 h, the amount of secreted TNF-α was still one third of the total TNF-α. Lipopolysaccharide (LPS), a known activator of immune cells also induced TNF-α production with similar kinetics as dCGN (Fig. 2B). However, the amount of TNF-α produced by LPS was 4-fold less than the one produced by dCGN and it was not detected after 8 hours of culture (Fig. 2B). Similarly, monocytic THP-1 cells cultivated in the presence of variable concentration of dCGN showed an increase in TNF-α production (Fig. 2C). This increase in TNF-α production was significantly smaller (about 10-fold) than the one presented by PBM (Fig. 2A). No TNF-α was released from THP-1 cells exposed to native CGN (not shown). TNF-α production by THP-1 cells was not dose dependent to the amount of dCGN used. Also there was no difference between the two forms (10 and 40 kDa) of dCGN (Fig. 2C). Interestingly, TNF-α release from THP-1 cells stimulated with dCGN reached a maximum level at 32 h, while stimulation with LPS reached a maximum level at 56 h (Fig. 2D).\n10.1371/journal.pone.0008666.g002 Figure 2 Degraded CGN stimulated TNF secretion from monocytes.\nLevels of TNF released from peripheral blood monocytes (A–B) and THP-1 cells (C–D) after stimulation with dCGN. A: TNF release induced by native CGN (open bars), 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). B: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares). C: TNF release induced by nothing (control; open bars), 10 µg/ml LPS (hatched bars), or increasing concentrations of 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). D: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares).\n\nE"}

GO-BP

pmc-enju-pas

bionlp-st-ge-2016-coref

{"project":"bionlp-st-ge-2016-coref","denotations":[{"id":"T7626","span":{"begin":957,"end":962},"obj":"Antecedent"},{"id":"T7623","span":{"begin":439,"end":445},"obj":"Anaphor"},{"id":"T7624","span":{"begin":340,"end":348},"obj":"Antecedent"},{"id":"T7625","span":{"begin":1000,"end":1007},"obj":"Anaphor"}],"relations":[{"id":"R6773","pred":"boundBy","subj":"T7623","obj":"T7624"},{"id":"R6774","pred":"boundBy","subj":"T7625","obj":"T7626"}],"namespaces":[{"prefix":"_base","uri":"https://bionlp.dbcls.jp/ontology/ge.owl#"}],"text":"Degraded CGN Induced-TNF-α Production by Monocytes In Vitro \nIn order to study the capacity of dCGN to stimulate TNF-α production, peripheral blood monocytes were cultivated in the presence of dCGN (0.1 to 1 mg/ml). Very low levels of TNF-α were induced in PBM after stimulation with native CGN (Fig. 2A). Addition of 0.1 mg/ml 10 kDa dCGN resulted in approximately a 60-fold increase in TNF-α production by PBM. This was a dose-dependent effect that reached a 180-fold increase when cells were exposed to 1 mg/ml of 10 kDa dCGN (Fig. 2A). A 250-fold increase in TNF-α production was detected at 1 mg/ml 40 kDa dCGN (Fig. 2A). TNF-α production increased in time reaching a maximum level at 8 hours of culture (Figure 2B). After 24 h, the amount of secreted TNF-α was still one third of the total TNF-α. Lipopolysaccharide (LPS), a known activator of immune cells also induced TNF-α production with similar kinetics as dCGN (Fig. 2B). However, the amount of TNF-α produced by LPS was 4-fold less than the one produced by dCGN and it was not detected after 8 hours of culture (Fig. 2B). Similarly, monocytic THP-1 cells cultivated in the presence of variable concentration of dCGN showed an increase in TNF-α production (Fig. 2C). This increase in TNF-α production was significantly smaller (about 10-fold) than the one presented by PBM (Fig. 2A). No TNF-α was released from THP-1 cells exposed to native CGN (not shown). TNF-α production by THP-1 cells was not dose dependent to the amount of dCGN used. Also there was no difference between the two forms (10 and 40 kDa) of dCGN (Fig. 2C). Interestingly, TNF-α release from THP-1 cells stimulated with dCGN reached a maximum level at 32 h, while stimulation with LPS reached a maximum level at 56 h (Fig. 2D).\n10.1371/journal.pone.0008666.g002 Figure 2 Degraded CGN stimulated TNF secretion from monocytes.\nLevels of TNF released from peripheral blood monocytes (A–B) and THP-1 cells (C–D) after stimulation with dCGN. A: TNF release induced by native CGN (open bars), 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). B: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares). C: TNF release induced by nothing (control; open bars), 10 µg/ml LPS (hatched bars), or increasing concentrations of 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). D: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares).\n\nE"}

bionlp-st-ge-2016-spacy-parsed

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"T7225","span":{"begin":142,"end":147},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"},{"id":"T15841","span":{"begin":1896,"end":1901},"obj":"http://purl.obolibrary.org/obo/UBERON_0000178"}],"text":"Degraded CGN Induced-TNF-α Production by Monocytes In Vitro \nIn order to study the capacity of dCGN to stimulate TNF-α production, peripheral blood monocytes were cultivated in the presence of dCGN (0.1 to 1 mg/ml). Very low levels of TNF-α were induced in PBM after stimulation with native CGN (Fig. 2A). Addition of 0.1 mg/ml 10 kDa dCGN resulted in approximately a 60-fold increase in TNF-α production by PBM. This was a dose-dependent effect that reached a 180-fold increase when cells were exposed to 1 mg/ml of 10 kDa dCGN (Fig. 2A). A 250-fold increase in TNF-α production was detected at 1 mg/ml 40 kDa dCGN (Fig. 2A). TNF-α production increased in time reaching a maximum level at 8 hours of culture (Figure 2B). After 24 h, the amount of secreted TNF-α was still one third of the total TNF-α. Lipopolysaccharide (LPS), a known activator of immune cells also induced TNF-α production with similar kinetics as dCGN (Fig. 2B). However, the amount of TNF-α produced by LPS was 4-fold less than the one produced by dCGN and it was not detected after 8 hours of culture (Fig. 2B). Similarly, monocytic THP-1 cells cultivated in the presence of variable concentration of dCGN showed an increase in TNF-α production (Fig. 2C). This increase in TNF-α production was significantly smaller (about 10-fold) than the one presented by PBM (Fig. 2A). No TNF-α was released from THP-1 cells exposed to native CGN (not shown). TNF-α production by THP-1 cells was not dose dependent to the amount of dCGN used. Also there was no difference between the two forms (10 and 40 kDa) of dCGN (Fig. 2C). Interestingly, TNF-α release from THP-1 cells stimulated with dCGN reached a maximum level at 32 h, while stimulation with LPS reached a maximum level at 56 h (Fig. 2D).\n10.1371/journal.pone.0008666.g002 Figure 2 Degraded CGN stimulated TNF secretion from monocytes.\nLevels of TNF released from peripheral blood monocytes (A–B) and THP-1 cells (C–D) after stimulation with dCGN. A: TNF release induced by native CGN (open bars), 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). B: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares). C: TNF release induced by nothing (control; open bars), 10 µg/ml LPS (hatched bars), or increasing concentrations of 10 kDa dCGN (grey bars), or 40 kDa dCGN (black bars). D: Kinetics of TNF release induced by nothing (control; black diamonds), 0.1 mg/ml 10 kDa dCGN (black triangles), 0.1 mg/ml 40 kDa dCGN (black squares), or 10 µg/ml LPS (open squares).\n\nE"}

sentences

events-check-again

bionlp-st-ge-2016-reference-tees

bionlp-st-ge-2016-reference

bionlp-st-ge-2016-uniprot

test2

PMC:2800179 / 17711-20327 JSONTXT

Annnotations TAB JSON ListView MergeView

PMC:2800179 / 17711-20327 JSON TXT