PubMed:26658904
Annnotations
Inflammaging
{"project":"Inflammaging","denotations":[{"id":"T1","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"T2","span":{"begin":110,"end":121},"obj":"Sentence"},{"id":"T3","span":{"begin":122,"end":276},"obj":"Sentence"},{"id":"T4","span":{"begin":277,"end":369},"obj":"Sentence"},{"id":"T5","span":{"begin":370,"end":531},"obj":"Sentence"},{"id":"T6","span":{"begin":532,"end":635},"obj":"Sentence"},{"id":"T7","span":{"begin":636,"end":776},"obj":"Sentence"},{"id":"T8","span":{"begin":777,"end":785},"obj":"Sentence"},{"id":"T9","span":{"begin":786,"end":941},"obj":"Sentence"},{"id":"T10","span":{"begin":942,"end":1022},"obj":"Sentence"},{"id":"T11","span":{"begin":1023,"end":1122},"obj":"Sentence"},{"id":"T12","span":{"begin":1123,"end":1266},"obj":"Sentence"},{"id":"T13","span":{"begin":1267,"end":1291},"obj":"Sentence"},{"id":"T14","span":{"begin":1292,"end":1398},"obj":"Sentence"},{"id":"T15","span":{"begin":1399,"end":1410},"obj":"Sentence"},{"id":"T16","span":{"begin":1411,"end":1464},"obj":"Sentence"},{"id":"T17","span":{"begin":1465,"end":1512},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"T2","span":{"begin":110,"end":121},"obj":"Sentence"},{"id":"T3","span":{"begin":122,"end":276},"obj":"Sentence"},{"id":"T4","span":{"begin":277,"end":369},"obj":"Sentence"},{"id":"T5","span":{"begin":370,"end":531},"obj":"Sentence"},{"id":"T6","span":{"begin":532,"end":635},"obj":"Sentence"},{"id":"T7","span":{"begin":636,"end":776},"obj":"Sentence"},{"id":"T8","span":{"begin":777,"end":785},"obj":"Sentence"},{"id":"T9","span":{"begin":786,"end":941},"obj":"Sentence"},{"id":"T10","span":{"begin":942,"end":1022},"obj":"Sentence"},{"id":"T11","span":{"begin":1023,"end":1122},"obj":"Sentence"},{"id":"T12","span":{"begin":1123,"end":1266},"obj":"Sentence"},{"id":"T13","span":{"begin":1267,"end":1291},"obj":"Sentence"},{"id":"T14","span":{"begin":1292,"end":1398},"obj":"Sentence"},{"id":"T15","span":{"begin":1399,"end":1410},"obj":"Sentence"},{"id":"T16","span":{"begin":1411,"end":1464},"obj":"Sentence"},{"id":"T17","span":{"begin":1465,"end":1512},"obj":"Sentence"}],"text":"Association of Killer Cell Immunoglobulin- Like Receptor Genes in Iranian Patients with Rheumatoid Arthritis.\nOBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by persistent synovitis, ultimately leading to cartilage and bone degeneration. Natural Killer cells and CD28 null T-cells are suspected as role players in RA pathogenesis. These cells are similar in feature and function, as they both exert their cytotoxic effect via Killer Cell Immunoglobulin- Like Receptors (KIR) on their surface. KIR genes have either an inhibitory or activating effect depending on their intracytoplasmic structure. Herein we genotyped 16 KIR genes, 3 pseudo genes and 6 HLA class І genes as their corresponding ligands in RA patients and control subjects.\nMETHODS: In this case-control study, KIR and HLA genes were genotyped in 400 RA patients and 372 matched healthy controls using sequence-specific primers (SSP-PCR). Differences in the frequency of genes and haplotypes were determined by χ² test.\nRESULTS: KIR2DL2, 2DL5a, 2DL5b and activating KIR: KIR2DS5 and 3DS1 were all protective against RA. KIR2DL5 removal from a full Inhibitory KIR haplotype converted the mild protection (OR = 0.56) to a powerful predisposition to RA (OR = 16.47). Inhibitory haplotype No. 7 comprising KIR2DL5 in the absence of KIR2DL1 and KIR2DL3 confers a 14-fold protective effect against RA.\nCONCLUSION: Individuals carrying the inhibitory KIR haplotype No. 6 have a high potential risk for developing RA."}
DisGeNET5_gene_disease
{"project":"DisGeNET5_gene_disease","denotations":[{"id":"26658904-2#25#29#gene940","span":{"begin":302,"end":306},"obj":"gene940"},{"id":"26658904-0#15#56#gene3806","span":{"begin":15,"end":56},"obj":"gene3806"},{"id":"26658904-0#15#56#gene3812","span":{"begin":15,"end":56},"obj":"gene3812"},{"id":"26658904-0#88#108#diseaseC0003873","span":{"begin":88,"end":108},"obj":"diseaseC0003873"},{"id":"26658904-10#13#20#gene57292","span":{"begin":1305,"end":1312},"obj":"gene57292"},{"id":"26658904-10#13#20#gene553128","span":{"begin":1305,"end":1312},"obj":"gene553128"},{"id":"26658904-10#39#46#gene3802","span":{"begin":1331,"end":1338},"obj":"gene3802"},{"id":"26658904-10#51#58#gene3804","span":{"begin":1343,"end":1350},"obj":"gene3804"},{"id":"26658904-10#103#105#diseaseC0003873","span":{"begin":1395,"end":1397},"obj":"diseaseC0003873"},{"id":"26658904-10#103#105#diseaseC0003873","span":{"begin":1395,"end":1397},"obj":"diseaseC0003873"},{"id":"26658904-2#76#78#diseaseC0003873","span":{"begin":353,"end":355},"obj":"diseaseC0003873"},{"id":"26658904-8#0#7#gene3803","span":{"begin":1032,"end":1039},"obj":"gene3803"},{"id":"26658904-8#42#49#gene3810","span":{"begin":1074,"end":1081},"obj":"gene3810"},{"id":"26658904-8#87#89#diseaseC0003873","span":{"begin":1119,"end":1121},"obj":"diseaseC0003873"}],"relations":[{"id":"15#56#gene380688#108#diseaseC0003873","pred":"associated_with","subj":"26658904-0#15#56#gene3806","obj":"26658904-0#88#108#diseaseC0003873"},{"id":"15#56#gene381288#108#diseaseC0003873","pred":"associated_with","subj":"26658904-0#15#56#gene3812","obj":"26658904-0#88#108#diseaseC0003873"},{"id":"13#20#gene57292103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#13#20#gene57292","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"13#20#gene57292103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#13#20#gene57292","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"13#20#gene553128103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#13#20#gene553128","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"13#20#gene553128103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#13#20#gene553128","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"39#46#gene3802103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#39#46#gene3802","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"39#46#gene3802103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#39#46#gene3802","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"51#58#gene3804103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#51#58#gene3804","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"51#58#gene3804103#105#diseaseC0003873","pred":"associated_with","subj":"26658904-10#51#58#gene3804","obj":"26658904-10#103#105#diseaseC0003873"},{"id":"25#29#gene94076#78#diseaseC0003873","pred":"associated_with","subj":"26658904-2#25#29#gene940","obj":"26658904-2#76#78#diseaseC0003873"},{"id":"0#7#gene380387#89#diseaseC0003873","pred":"associated_with","subj":"26658904-8#0#7#gene3803","obj":"26658904-8#87#89#diseaseC0003873"},{"id":"42#49#gene381087#89#diseaseC0003873","pred":"associated_with","subj":"26658904-8#42#49#gene3810","obj":"26658904-8#87#89#diseaseC0003873"}],"text":"Association of Killer Cell Immunoglobulin- Like Receptor Genes in Iranian Patients with Rheumatoid Arthritis.\nOBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by persistent synovitis, ultimately leading to cartilage and bone degeneration. Natural Killer cells and CD28 null T-cells are suspected as role players in RA pathogenesis. These cells are similar in feature and function, as they both exert their cytotoxic effect via Killer Cell Immunoglobulin- Like Receptors (KIR) on their surface. KIR genes have either an inhibitory or activating effect depending on their intracytoplasmic structure. Herein we genotyped 16 KIR genes, 3 pseudo genes and 6 HLA class І genes as their corresponding ligands in RA patients and control subjects.\nMETHODS: In this case-control study, KIR and HLA genes were genotyped in 400 RA patients and 372 matched healthy controls using sequence-specific primers (SSP-PCR). Differences in the frequency of genes and haplotypes were determined by χ² test.\nRESULTS: KIR2DL2, 2DL5a, 2DL5b and activating KIR: KIR2DS5 and 3DS1 were all protective against RA. KIR2DL5 removal from a full Inhibitory KIR haplotype converted the mild protection (OR = 0.56) to a powerful predisposition to RA (OR = 16.47). Inhibitory haplotype No. 7 comprising KIR2DL5 in the absence of KIR2DL1 and KIR2DL3 confers a 14-fold protective effect against RA.\nCONCLUSION: Individuals carrying the inhibitory KIR haplotype No. 6 have a high potential risk for developing RA."}
DisGeNet-2017-sample
{"project":"DisGeNet-2017-sample","denotations":[{"id":"T978","span":{"begin":1305,"end":1312},"obj":"gene:57292"},{"id":"T979","span":{"begin":1395,"end":1397},"obj":"disease:C0003873"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T978","obj":"T979"},{"id":"R2","pred":"associated_with","subj":"T978","obj":"T979"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Association of Killer Cell Immunoglobulin- Like Receptor Genes in Iranian Patients with Rheumatoid Arthritis.\nOBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by persistent synovitis, ultimately leading to cartilage and bone degeneration. Natural Killer cells and CD28 null T-cells are suspected as role players in RA pathogenesis. These cells are similar in feature and function, as they both exert their cytotoxic effect via Killer Cell Immunoglobulin- Like Receptors (KIR) on their surface. KIR genes have either an inhibitory or activating effect depending on their intracytoplasmic structure. Herein we genotyped 16 KIR genes, 3 pseudo genes and 6 HLA class І genes as their corresponding ligands in RA patients and control subjects.\nMETHODS: In this case-control study, KIR and HLA genes were genotyped in 400 RA patients and 372 matched healthy controls using sequence-specific primers (SSP-PCR). Differences in the frequency of genes and haplotypes were determined by χ² test.\nRESULTS: KIR2DL2, 2DL5a, 2DL5b and activating KIR: KIR2DS5 and 3DS1 were all protective against RA. KIR2DL5 removal from a full Inhibitory KIR haplotype converted the mild protection (OR = 0.56) to a powerful predisposition to RA (OR = 16.47). Inhibitory haplotype No. 7 comprising KIR2DL5 in the absence of KIR2DL1 and KIR2DL3 confers a 14-fold protective effect against RA.\nCONCLUSION: Individuals carrying the inhibitory KIR haplotype No. 6 have a high potential risk for developing RA."}
sentences
{"project":"sentences","denotations":[{"id":"TextSentencer_T1","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"TextSentencer_T2","span":{"begin":110,"end":121},"obj":"Sentence"},{"id":"TextSentencer_T3","span":{"begin":122,"end":276},"obj":"Sentence"},{"id":"TextSentencer_T4","span":{"begin":277,"end":369},"obj":"Sentence"},{"id":"TextSentencer_T5","span":{"begin":370,"end":531},"obj":"Sentence"},{"id":"TextSentencer_T6","span":{"begin":532,"end":635},"obj":"Sentence"},{"id":"TextSentencer_T7","span":{"begin":636,"end":776},"obj":"Sentence"},{"id":"TextSentencer_T8","span":{"begin":777,"end":785},"obj":"Sentence"},{"id":"TextSentencer_T9","span":{"begin":786,"end":941},"obj":"Sentence"},{"id":"TextSentencer_T10","span":{"begin":942,"end":1022},"obj":"Sentence"},{"id":"TextSentencer_T11","span":{"begin":1023,"end":1122},"obj":"Sentence"},{"id":"TextSentencer_T12","span":{"begin":1123,"end":1266},"obj":"Sentence"},{"id":"TextSentencer_T13","span":{"begin":1267,"end":1291},"obj":"Sentence"},{"id":"TextSentencer_T14","span":{"begin":1292,"end":1398},"obj":"Sentence"},{"id":"TextSentencer_T15","span":{"begin":1399,"end":1410},"obj":"Sentence"},{"id":"TextSentencer_T16","span":{"begin":1411,"end":1464},"obj":"Sentence"},{"id":"TextSentencer_T17","span":{"begin":1465,"end":1512},"obj":"Sentence"},{"id":"T1","span":{"begin":0,"end":109},"obj":"Sentence"},{"id":"T2","span":{"begin":110,"end":121},"obj":"Sentence"},{"id":"T3","span":{"begin":122,"end":276},"obj":"Sentence"},{"id":"T4","span":{"begin":277,"end":369},"obj":"Sentence"},{"id":"T5","span":{"begin":370,"end":531},"obj":"Sentence"},{"id":"T6","span":{"begin":532,"end":635},"obj":"Sentence"},{"id":"T7","span":{"begin":636,"end":776},"obj":"Sentence"},{"id":"T8","span":{"begin":777,"end":785},"obj":"Sentence"},{"id":"T9","span":{"begin":786,"end":941},"obj":"Sentence"},{"id":"T10","span":{"begin":942,"end":1022},"obj":"Sentence"},{"id":"T11","span":{"begin":1023,"end":1122},"obj":"Sentence"},{"id":"T12","span":{"begin":1123,"end":1266},"obj":"Sentence"},{"id":"T13","span":{"begin":1267,"end":1291},"obj":"Sentence"},{"id":"T14","span":{"begin":1292,"end":1398},"obj":"Sentence"},{"id":"T15","span":{"begin":1399,"end":1410},"obj":"Sentence"},{"id":"T16","span":{"begin":1411,"end":1464},"obj":"Sentence"},{"id":"T17","span":{"begin":1465,"end":1512},"obj":"Sentence"}],"namespaces":[{"prefix":"_base","uri":"http://pubannotation.org/ontology/tao.owl#"}],"text":"Association of Killer Cell Immunoglobulin- Like Receptor Genes in Iranian Patients with Rheumatoid Arthritis.\nOBJECTIVES: Rheumatoid arthritis (RA) is a chronic inflammatory disorder characterized by persistent synovitis, ultimately leading to cartilage and bone degeneration. Natural Killer cells and CD28 null T-cells are suspected as role players in RA pathogenesis. These cells are similar in feature and function, as they both exert their cytotoxic effect via Killer Cell Immunoglobulin- Like Receptors (KIR) on their surface. KIR genes have either an inhibitory or activating effect depending on their intracytoplasmic structure. Herein we genotyped 16 KIR genes, 3 pseudo genes and 6 HLA class І genes as their corresponding ligands in RA patients and control subjects.\nMETHODS: In this case-control study, KIR and HLA genes were genotyped in 400 RA patients and 372 matched healthy controls using sequence-specific primers (SSP-PCR). Differences in the frequency of genes and haplotypes were determined by χ² test.\nRESULTS: KIR2DL2, 2DL5a, 2DL5b and activating KIR: KIR2DS5 and 3DS1 were all protective against RA. KIR2DL5 removal from a full Inhibitory KIR haplotype converted the mild protection (OR = 0.56) to a powerful predisposition to RA (OR = 16.47). Inhibitory haplotype No. 7 comprising KIR2DL5 in the absence of KIR2DL1 and KIR2DL3 confers a 14-fold protective effect against RA.\nCONCLUSION: Individuals carrying the inhibitory KIR haplotype No. 6 have a high potential risk for developing RA."}