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Fact | preserve | 1738-1747 | 1738-1747 | T109 | influence | AFFECTS | 1,738 | 1,747 | preserve | 1735-1737 | 1735-1737 | T104 | GC | Hormone | 1,735 | 1,737 | preserve | 1748-1750 | 1748-1750 | T105 | DC | Cell | 1,748 | 1,750 | A2 | The results indicate that GC influence DC development and function in vitro as well as in vivo. | 1703-1804 | 1,703 | 1,804 | The results indicate that @SUBJECT$ @PREDICAT$ @OBJECT$ development and function in vitro as well as in vivo. |
Probable | preserve | 243-245 | 243-245 | T16 | in | TREATS | 243 | 245 | preserve | 202-217 | 202-217 | T11 | Glucocorticoids | Hormone | 202 | 217 | preserve | 252-261 | 252-261 | T13 | asthmatic | DiseaseOrSyndrome | 252 | 261 | A3 | Glucocorticoids (GC) are frequently used in asthmatic patients. | 202-271 | 202 | 271 | @SUBJECT$ (GC) are frequently used @PREDICAT$ @OBJECT$ patients. |
Fact | preserve | 927-931 | 927-931 | T60 | with | PROCESS_OF | 927 | 931 | preserve | 937-959 | 953-959 | T59 | moderate atopic asthma | Finding | 937 | 959 | preserve | 918-926 | 918-926 | T56 | patients | PatientOrDisabledGroup | 918 | 926 | A4 | To study the effect of GC in vivo patients with mild/moderate atopic asthma were selected. | 878-974 | 878 | 974 | To study the effect of GC in vivo @OBJECT$ @PREDICAT$ mild/ @SUBJECT$ were selected. |
Fact | preserve | 252-270 | 262-270 | T15 | asthmatic patients | PROCESS_OF | 252 | 270 | preserve | 252-261 | 252-261 | T13 | asthmatic | DiseaseOrSyndrome | 252 | 261 | preserve | 262-270 | 262-270 | T14 | patients | PatientOrDisabledGroup | 262 | 270 | A6 | Glucocorticoids (GC) are frequently used in asthmatic patients. | 202-271 | 202 | 271 | Glucocorticoids (GC) are frequently used in @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 16-24 | 16-24 | T5 | modulate | AFFECTS | 16 | 24 | preserve | 0-15 | 0-15 | T1 | Glucocorticoids | Hormone | 0 | 15 | preserve | 44-59 | 54-59 | T3 | dendritic cells | Cell | 44 | 59 | A7 | Glucocorticoids modulate the development of dendritic cells from blood precursors. | 0-88 | 0 | 88 | @SUBJECT$ @PREDICAT$ the development of @OBJECT$ from blood precursors. |
Probable | preserve | 243-245 | 243-245 | T16 | in | TREATS | 243 | 245 | preserve | 202-217 | 202-217 | T11 | Glucocorticoids | Hormone | 202 | 217 | preserve | 262-270 | 262-270 | T14 | patients | PatientOrDisabledGroup | 262 | 270 | A8 | Glucocorticoids (GC) are frequently used in asthmatic patients. | 202-271 | 202 | 271 | @SUBJECT$ (GC) are frequently used @PREDICAT$ asthmatic @OBJECT$ . |
Fact | preserve | 1738-1747 | 1738-1747 | T112 | Treatment | TREATS | 1,738 | 1,747 | preserve | 1768-1774 | 1768-1774 | T106 | IL-1Ra | AminoAcidPeptideOrProtein | 1,768 | 1,774 | preserve | 1754-1762 | 1754-1762 | T105 | patients | PatientOrDisabledGroup | 1,754 | 1,762 | A1 | Treatment of RA patients with IL-1Ra (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. | 1738-1909 | 1,738 | 1,909 | @PREDICAT$ of RA @OBJECT$ with @SUBJECT$ (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. |
Fact | preserve | 2322-2333 | 2325-2333 | T143 | RA patients | PROCESS_OF | 2,322 | 2,333 | preserve | 2322-2324 | 2322-2324 | T137 | RA | DiseaseOrSyndrome | 2,322 | 2,324 | preserve | 2325-2333 | 2325-2333 | T138 | patients | PatientOrDisabledGroup | 2,325 | 2,333 | A2 | Similar to the response in adjuvant arthritic rats, RA patients treated with IL-1Ra showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. | 2270-2477 | 2,270 | 2,477 | Similar to the response in adjuvant arthritic rats, @SUBJECT$ @PREDICAT$ @OBJECT$ treated with IL-1Ra showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. |
Fact | preserve | 1365-1372 | 1365-1372 | T84 | treated | TREATS | 1,365 | 1,372 | preserve | 1378-1384 | 1378-1384 | T82 | IL-1Ra | AminoAcidPeptideOrProtein | 1,378 | 1,384 | preserve | 1360-1364 | 1360-1364 | T81 | rats | Mammal | 1,360 | 1,364 | A3 | Modest antiinflammatory effects were observed in the adjuvant arthritis rats treated with IL-1Ra. | 1282-1385 | 1,282 | 1,385 | Modest antiinflammatory effects were observed in the adjuvant arthritis @OBJECT$ @PREDICAT$ with @SUBJECT$ . |
Fact | preserve | 2235-2237 | 2235-2237 | T132 | in | PROCESS_OF | 2,235 | 2,237 | preserve | 2215-2234 | 2223-2234 | T129 | disease progression | PathologicFunction | 2,215 | 2,234 | preserve | 2242-2268 | 2259-2268 | T131 | collagen-induced arthritis | ExperimentalModelOfDisease | 2,242 | 2,268 | A4 | In contrast, IL-1 is of major importance in mediating all aspects of disease progression in rat collagen-induced arthritis. | 2140-2269 | 2,140 | 2,269 | In contrast, IL-1 is of major importance in mediating all aspects of @SUBJECT$ @PREDICAT$ rat @OBJECT$ . |
Fact | preserve | 764-766 | 764-766 | T58 | in | TREATS | 764 | 766 | preserve | 754-763 | 754-763 | T44 | treatment | TherapeuticOrPreventiveProcedure | 754 | 763 | preserve | 771-775 | 771-775 | T45 | rats | Mammal | 771 | 775 | A5 | The effects of treatment in the rats were monitored by sequential caliper measurement of the ankle joints, determination of final paw weights, and histologic evaluation with particular emphasis on bone and cartilage lesions. | 739-981 | 739 | 981 | The effects of @SUBJECT$ @PREDICAT$ the @OBJECT$ were monitored by sequential caliper measurement of the ankle joints, determination of final paw weights, and histologic evaluation with particular emphasis on bone and cartilage lesions. |
Fact | preserve | 2334-2341 | 2334-2341 | T144 | treated | TREATS | 2,334 | 2,341 | preserve | 2353-2359 | 2353-2359 | T139 | IL-1Ra | AminoAcidPeptideOrProtein | 2,353 | 2,359 | preserve | 2322-2324 | 2322-2324 | T137 | RA | DiseaseOrSyndrome | 2,322 | 2,324 | A6 | Similar to the response in adjuvant arthritic rats, RA patients treated with IL-1Ra showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. | 2270-2477 | 2,270 | 2,477 | Similar to the response in adjuvant arthritic rats, @OBJECT$ patients @PREDICAT$ with @SUBJECT$ showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. |
Fact | preserve | 1738-1747 | 1738-1747 | T112 | Treatment | TREATS | 1,738 | 1,747 | preserve | 1768-1774 | 1768-1774 | T106 | IL-1Ra | AminoAcidPeptideOrProtein | 1,768 | 1,774 | preserve | 1751-1753 | 1751-1753 | T104 | RA | DiseaseOrSyndrome | 1,751 | 1,753 | A7 | Treatment of RA patients with IL-1Ra (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. | 1738-1909 | 1,738 | 1,909 | @PREDICAT$ of @OBJECT$ patients with @SUBJECT$ (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. |
Fact | preserve | 986-993 | 986-993 | T70 | effects | AFFECTS | 986 | 993 | preserve | 997-1003 | 997-1003 | T60 | IL-1Ra | AminoAcidPeptideOrProtein | 997 | 1,003 | preserve | 1007-1021 | 1013-1021 | T61 | joint swelling | SignOrSymptom | 1,007 | 1,021 | A8 | The effects of IL-1Ra on joint swelling and radiographic bone damage in patients with rheumatoid arthritis (RA) in a 6-month trial were compared with the findings in rats. | 982-1165 | 982 | 1,165 | The @PREDICAT$ of @SUBJECT$ on @OBJECT$ and radiographic bone damage in patients with rheumatoid arthritis (RA) in a 6-month trial were compared with the findings in rats. |
Fact | preserve | 1069-1073 | 1069-1073 | T72 | with | PROCESS_OF | 1,069 | 1,073 | preserve | 1074-1094 | 1085-1094 | T65 | rheumatoid arthritis | DiseaseOrSyndrome | 1,074 | 1,094 | preserve | 1060-1068 | 1060-1068 | T64 | patients | PatientOrDisabledGroup | 1,060 | 1,068 | A9 | The effects of IL-1Ra on joint swelling and radiographic bone damage in patients with rheumatoid arthritis (RA) in a 6-month trial were compared with the findings in rats. | 982-1165 | 982 | 1,165 | The effects of IL-1Ra on joint swelling and radiographic bone damage in @OBJECT$ @PREDICAT$ @SUBJECT$ (RA) in a 6-month trial were compared with the findings in rats. |
Uncommitted | preserve | 210-214 | 210-214 | T23 | role | AFFECTS | 210 | 214 | preserve | 218-251 | 241-251 | T13 | interleukin-1 receptor antagonist | AminoAcidPeptideOrProtein | 218 | 251 | preserve | 309-335 | 326-335 | T18 | collagen-induced arthritis | ExperimentalModelOfDisease | 309 | 335 | A10 | OBJECTIVE: To determine the role of interleukin-1 receptor antagonist (IL-1Ra) in rat adjuvant arthritis and rat type II collagen-induced arthritis, and to compare the efficacy in rat models with that seen in human clinical trials of IL-1Ra. | 182-435 | 182 | 435 | OBJECTIVE: To determine the @PREDICAT$ of @SUBJECT$ (IL-1Ra) in rat adjuvant arthritis and rat type II @OBJECT$ , and to compare the efficacy in rat models with that seen in human clinical trials of IL-1Ra. |
Probable | preserve | 1970-1979 | 1970-1979 | T123 | mediating | ASSOCIATED_WITH | 1,970 | 1,979 | preserve | 1922-1926 | 1922-1926 | T115 | IL-1 | AminoAcidPeptideOrProtein | 1,922 | 1,926 | preserve | 1984-1999 | 1989-1999 | T117 | bone resorption | OrganOrTissueFunction | 1,984 | 1,999 | A11 | CONCLUSION: IL-1 appears to be of major importance in mediating the bone resorption that occurs in rat adjuvant arthritis, but is less important in the pathogenesis of periarticular inflammation in this disease. | 1910-2139 | 1,910 | 2,139 | CONCLUSION: @SUBJECT$ appears to be of major importance in @PREDICAT$ the @OBJECT$ that occurs in rat adjuvant arthritis, but is less important in the pathogenesis of periarticular inflammation in this disease. |
Fact | preserve | 539-546 | 539-546 | T40 | treated | TREATS | 539 | 546 | preserve | 552-558 | 552-558 | T30 | IL-1Ra | AminoAcidPeptideOrProtein | 552 | 558 | preserve | 466-484 | 475-484 | T27 | adjuvant arthritis | ExperimentalModelOfDisease | 466 | 484 | A13 | METHODS: Rats with developing adjuvant arthritis or established collagen-induced arthritis were treated with IL-1Ra by continuous infusion in order to determine and maintain efficacious blood levels of this IL-1 inhibitory protein in the rats for comparison with human clinical data. | 436-738 | 436 | 738 | METHODS: Rats with developing @OBJECT$ or established collagen-induced arthritis were @PREDICAT$ with @SUBJECT$ by continuous infusion in order to determine and maintain efficacious blood levels of this IL-1 inhibitory protein in the rats for comparison with human clinical data. |
Fact | preserve | 2334-2341 | 2334-2341 | T144 | treated | TREATS | 2,334 | 2,341 | preserve | 2353-2359 | 2353-2359 | T139 | IL-1Ra | AminoAcidPeptideOrProtein | 2,353 | 2,359 | preserve | 2325-2333 | 2325-2333 | T138 | patients | PatientOrDisabledGroup | 2,325 | 2,333 | A15 | Similar to the response in adjuvant arthritic rats, RA patients treated with IL-1Ra showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. | 2270-2477 | 2,270 | 2,477 | Similar to the response in adjuvant arthritic rats, RA @OBJECT$ @PREDICAT$ with @SUBJECT$ showed only modest antiinflammatory activity, but had evidence of inhibition of progression of bone resorption. |
Fact | preserve | 2123-2125 | 2123-2125 | T125 | in | COEXISTS_WITH | 2,123 | 2,125 | preserve | 2110-2122 | 2110-2122 | T121 | inflammation | PathologicFunction | 2,110 | 2,122 | preserve | 2131-2138 | 2131-2138 | T122 | disease | DiseaseOrSyndrome | 2,131 | 2,138 | A16 | CONCLUSION: IL-1 appears to be of major importance in mediating the bone resorption that occurs in rat adjuvant arthritis, but is less important in the pathogenesis of periarticular inflammation in this disease. | 1910-2139 | 1,910 | 2,139 | CONCLUSION: IL-1 appears to be of major importance in mediating the bone resorption that occurs in rat adjuvant arthritis, but is less important in the pathogenesis of periarticular @SUBJECT$ @PREDICAT$ this @OBJECT$ . |
Fact | preserve | 1328-1330 | 1328-1330 | T83 | in | PROCESS_OF | 1,328 | 1,330 | preserve | 1289-1313 | 1306-1313 | T79 | antiinflammatory effects | PhysiologicFunction | 1,289 | 1,313 | preserve | 1360-1364 | 1360-1364 | T81 | rats | Mammal | 1,360 | 1,364 | A17 | Modest antiinflammatory effects were observed in the adjuvant arthritis rats treated with IL-1Ra. | 1282-1385 | 1,282 | 1,385 | Modest @SUBJECT$ were observed @PREDICAT$ the adjuvant arthritis @OBJECT$ treated with IL-1Ra. |
Fact | preserve | 72-74 | 72-74 | T10 | in | LOCATION_OF | 72 | 74 | preserve | 75-94 | 88-94 | T5 | animal models | Animal | 75 | 94 | preserve | 38-71 | 61-71 | T4 | interleukin-1 receptor antagonist | AminoAcidPeptideOrProtein | 38 | 71 | A19 | Efficacy of sustained blood levels of interleukin-1 receptor antagonist in animal models of arthritis: comparison of efficacy in animal models with human clinical data. | 0-181 | 0 | 181 | Efficacy of sustained blood levels of @OBJECT$ @PREDICAT$ @SUBJECT$ of arthritis: comparison of efficacy in animal models with human clinical data. |
Fact | preserve | 2675-2677 | 2675-2677 | T160 | in | LOCATION_OF | 2,675 | 2,677 | preserve | 2678-2684 | 2678-2684 | T155 | humans | Human | 2,678 | 2,684 | preserve | 2633-2647 | 2638-2647 | T153 | IL-1 receptors | AminoAcidPeptideOrProtein | 2,633 | 2,647 | A20 | However, a comparison of the plasma levels of IL-1Ra in humans and rats suggests that the optimal level of dosing for continuous saturation of IL-1 receptors may not have been achieved in humans, although this was achieved in the rat studies. | 2478-2738 | 2,478 | 2,738 | However, a comparison of the plasma levels of IL-1Ra in humans and rats suggests that the optimal level of dosing for continuous saturation of @OBJECT$ may not have been achieved @PREDICAT$ @SUBJECT$ , although this was achieved in the rat studies. |
Uncommitted | preserve | 210-214 | 210-214 | T23 | role | AFFECTS | 210 | 214 | preserve | 218-251 | 241-251 | T13 | interleukin-1 receptor antagonist | AminoAcidPeptideOrProtein | 218 | 251 | preserve | 274-292 | 283-292 | T15 | adjuvant arthritis | ExperimentalModelOfDisease | 274 | 292 | A21 | OBJECTIVE: To determine the role of interleukin-1 receptor antagonist (IL-1Ra) in rat adjuvant arthritis and rat type II collagen-induced arthritis, and to compare the efficacy in rat models with that seen in human clinical trials of IL-1Ra. | 182-435 | 182 | 435 | OBJECTIVE: To determine the @PREDICAT$ of @SUBJECT$ (IL-1Ra) in rat @OBJECT$ and rat type II collagen-induced arthritis, and to compare the efficacy in rat models with that seen in human clinical trials of IL-1Ra. |
Fact | preserve | 539-546 | 539-546 | T40 | treated | TREATS | 539 | 546 | preserve | 552-558 | 552-558 | T30 | IL-1Ra | AminoAcidPeptideOrProtein | 552 | 558 | preserve | 500-533 | 524-533 | T29 | collagen-induced arthritis | ExperimentalModelOfDisease | 500 | 533 | A25 | METHODS: Rats with developing adjuvant arthritis or established collagen-induced arthritis were treated with IL-1Ra by continuous infusion in order to determine and maintain efficacious blood levels of this IL-1 inhibitory protein in the rats for comparison with human clinical data. | 436-738 | 436 | 738 | METHODS: Rats with developing adjuvant arthritis or established @OBJECT$ were @PREDICAT$ with @SUBJECT$ by continuous infusion in order to determine and maintain efficacious blood levels of this IL-1 inhibitory protein in the rats for comparison with human clinical data. |
Fact | preserve | 1751-1762 | 1754-1762 | T113 | RA patients | PROCESS_OF | 1,751 | 1,762 | preserve | 1751-1753 | 1751-1753 | T104 | RA | DiseaseOrSyndrome | 1,751 | 1,753 | preserve | 1754-1762 | 1754-1762 | T105 | patients | PatientOrDisabledGroup | 1,754 | 1,762 | A27 | Treatment of RA patients with IL-1Ra (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. | 1738-1909 | 1,738 | 1,909 | Treatment of @SUBJECT$ @PREDICAT$ @OBJECT$ with IL-1Ra (150 mg daily) resulted in modest inhibition of joint swelling and inhibition of radiographic progression of bone lesions. |
Fact | preserve | 1106-1110 | 1106-1110 | T82 | from | LOCATION_OF | 1,106 | 1,110 | preserve | 1117-1126 | 1117-1126 | T78 | microglia | Cell | 1,117 | 1,126 | preserve | 1092-1094 | 1092-1094 | T76 | NO | BiologicallyActiveSubstance | 1,092 | 1,094 | A2 | The results suggest that the mechanism by which indomethacin might be beneficial in treatment of AD might be due to the inhibition IL-1 and NO production from microglia. | 940-1127 | 940 | 1,127 | The results suggest that the mechanism by which indomethacin might be beneficial in treatment of AD might be due to the inhibition IL-1 and @OBJECT$ production @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 416-418 | 416-418 | T36 | on | LOCATION_OF | 416 | 418 | preserve | 423-432 | 423-432 | T29 | microglia | Cell | 423 | 432 | preserve | 366-393 | 388-393 | T26 | tumor necrosis factor alpha | AminoAcidPeptideOrProtein | 366 | 393 | A3 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), @OBJECT$ and nitric oxide (NO) @PREDICAT$ rat @SUBJECT$ in vitro were investigated. |
Uncommitted | preserve | 284-291 | 284-291 | T32 | Effects | INTERACTS_WITH | 284 | 291 | preserve | 295-307 | 295-307 | T23 | indomethacin | OrganicChemical | 295 | 307 | preserve | 337-350 | 337-350 | T25 | interleukin-1 | AminoAcidPeptideOrProtein | 337 | 350 | A5 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | @PREDICAT$ of @SUBJECT$ on proinflammatory cytokines @OBJECT$ (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. |
Fact | preserve | 707-716 | 707-716 | T59 | inhibited | INHIBITS | 707 | 716 | preserve | 694-706 | 694-706 | T52 | Indomethacin | OrganicChemical | 694 | 706 | preserve | 726-728 | 726-728 | T54 | NO | BiologicallyActiveSubstance | 726 | 728 | A6 | Indomethacin inhibited IL-1 and NO production by rat microglia stimulated at the concentration of 0.1-10 micromol/l. | 694-817 | 694 | 817 | @SUBJECT$ @PREDICAT$ IL-1 and @OBJECT$ production by rat microglia stimulated at the concentration of 0.1-10 micromol/l. |
Uncommitted | preserve | 284-291 | 284-291 | T32 | Effects | INTERACTS_WITH | 284 | 291 | preserve | 295-307 | 295-307 | T23 | indomethacin | OrganicChemical | 295 | 307 | preserve | 398-410 | 405-410 | T27 | nitric oxide | BiologicallyActiveSubstance | 398 | 410 | A7 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | @PREDICAT$ of @SUBJECT$ on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and @OBJECT$ (NO) on rat microglia in vitro were investigated. |
Fact | preserve | 86-88 | 86-88 | T13 | in | LOCATION_OF | 86 | 88 | preserve | 93-102 | 93-102 | T8 | microglia | Cell | 93 | 102 | preserve | 56-68 | 63-68 | T5 | nitric oxide | BiologicallyActiveSubstance | 56 | 68 | A8 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in rat microglia in vitro. | 0-112 | 0 | 112 | Inhibitory effects of indomethacin on interleukin-1 and @OBJECT$ production @PREDICAT$ rat @SUBJECT$ in vitro. |
Fact | preserve | 419-432 | 423-432 | T35 | rat microglia | PART_OF | 419 | 432 | preserve | 423-432 | 423-432 | T29 | microglia | Cell | 423 | 432 | preserve | 419-422 | 419-422 | T28 | rat | Mammal | 419 | 422 | A9 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on @OBJECT$ @PREDICAT$ @SUBJECT$ in vitro were investigated. |
Fact | preserve | 743-756 | 747-756 | T61 | rat microglia | PART_OF | 743 | 756 | preserve | 747-756 | 747-756 | T57 | microglia | Cell | 747 | 756 | preserve | 743-746 | 743-746 | T56 | rat | Mammal | 743 | 746 | A10 | Indomethacin inhibited IL-1 and NO production by rat microglia stimulated at the concentration of 0.1-10 micromol/l. | 694-817 | 694 | 817 | Indomethacin inhibited IL-1 and NO production by @OBJECT$ @PREDICAT$ @SUBJECT$ stimulated at the concentration of 0.1-10 micromol/l. |
Fact | preserve | 327-350 | 337-350 | T31 | cytokines interleukin-1 | ISA | 327 | 350 | preserve | 337-350 | 337-350 | T25 | interleukin-1 | AminoAcidPeptideOrProtein | 337 | 350 | preserve | 327-336 | 327-336 | T24 | cytokines | AminoAcidPeptideOrProtein | 327 | 336 | A11 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | Effects of indomethacin on proinflammatory @OBJECT$ @PREDICAT$ @SUBJECT$ (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. |
Fact | preserve | 11-18 | 11-18 | T10 | effects | INTERACTS_WITH | 11 | 18 | preserve | 22-34 | 22-34 | T3 | indomethacin | OrganicChemical | 22 | 34 | preserve | 56-68 | 63-68 | T5 | nitric oxide | BiologicallyActiveSubstance | 56 | 68 | A13 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in rat microglia in vitro. | 0-112 | 0 | 112 | Inhibitory @PREDICAT$ of @SUBJECT$ on interleukin-1 and @OBJECT$ production in rat microglia in vitro. |
Fact | preserve | 1106-1110 | 1106-1110 | T82 | from | LOCATION_OF | 1,106 | 1,110 | preserve | 1117-1126 | 1117-1126 | T78 | microglia | Cell | 1,117 | 1,126 | preserve | 1083-1087 | 1083-1087 | T75 | IL-1 | AminoAcidPeptideOrProtein | 1,083 | 1,087 | A14 | The results suggest that the mechanism by which indomethacin might be beneficial in treatment of AD might be due to the inhibition IL-1 and NO production from microglia. | 940-1127 | 940 | 1,127 | The results suggest that the mechanism by which indomethacin might be beneficial in treatment of AD might be due to the inhibition @OBJECT$ and NO production @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 416-418 | 416-418 | T36 | on | LOCATION_OF | 416 | 418 | preserve | 423-432 | 423-432 | T29 | microglia | Cell | 423 | 432 | preserve | 398-410 | 405-410 | T27 | nitric oxide | BiologicallyActiveSubstance | 398 | 410 | A16 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and @OBJECT$ (NO) @PREDICAT$ rat @SUBJECT$ in vitro were investigated. |
Fact | preserve | 416-418 | 416-418 | T36 | on | LOCATION_OF | 416 | 418 | preserve | 423-432 | 423-432 | T29 | microglia | Cell | 423 | 432 | preserve | 337-350 | 337-350 | T25 | interleukin-1 | AminoAcidPeptideOrProtein | 337 | 350 | A17 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | Effects of indomethacin on proinflammatory cytokines @OBJECT$ (IL-1), tumor necrosis factor alpha and nitric oxide (NO) @PREDICAT$ rat @SUBJECT$ in vitro were investigated. |
Fact | preserve | 11-18 | 11-18 | T10 | effects | INTERACTS_WITH | 11 | 18 | preserve | 22-34 | 22-34 | T3 | indomethacin | OrganicChemical | 22 | 34 | preserve | 38-51 | 38-51 | T4 | interleukin-1 | AminoAcidPeptideOrProtein | 38 | 51 | A18 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in rat microglia in vitro. | 0-112 | 0 | 112 | Inhibitory @PREDICAT$ of @SUBJECT$ on @OBJECT$ and nitric oxide production in rat microglia in vitro. |
Fact | preserve | 89-102 | 93-102 | T12 | rat microglia | PART_OF | 89 | 102 | preserve | 93-102 | 93-102 | T8 | microglia | Cell | 93 | 102 | preserve | 89-92 | 89-92 | T7 | rat | Mammal | 89 | 92 | A19 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in rat microglia in vitro. | 0-112 | 0 | 112 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in @OBJECT$ @PREDICAT$ @SUBJECT$ in vitro. |
Uncommitted | preserve | 284-291 | 284-291 | T32 | Effects | INTERACTS_WITH | 284 | 291 | preserve | 295-307 | 295-307 | T23 | indomethacin | OrganicChemical | 295 | 307 | preserve | 366-393 | 388-393 | T26 | tumor necrosis factor alpha | AminoAcidPeptideOrProtein | 366 | 393 | A20 | Effects of indomethacin on proinflammatory cytokines interleukin-1 (IL-1), tumor necrosis factor alpha and nitric oxide (NO) on rat microglia in vitro were investigated. | 284-467 | 284 | 467 | @PREDICAT$ of @SUBJECT$ on proinflammatory cytokines interleukin-1 (IL-1), @OBJECT$ and nitric oxide (NO) on rat microglia in vitro were investigated. |
Fact | preserve | 86-88 | 86-88 | T13 | in | LOCATION_OF | 86 | 88 | preserve | 93-102 | 93-102 | T8 | microglia | Cell | 93 | 102 | preserve | 38-51 | 38-51 | T4 | interleukin-1 | AminoAcidPeptideOrProtein | 38 | 51 | A21 | Inhibitory effects of indomethacin on interleukin-1 and nitric oxide production in rat microglia in vitro. | 0-112 | 0 | 112 | Inhibitory effects of indomethacin on @OBJECT$ and nitric oxide production @PREDICAT$ rat @SUBJECT$ in vitro. |
Fact | preserve | 707-716 | 707-716 | T59 | inhibited | INHIBITS | 707 | 716 | preserve | 694-706 | 694-706 | T52 | Indomethacin | OrganicChemical | 694 | 706 | preserve | 717-721 | 717-721 | T53 | IL-1 | AminoAcidPeptideOrProtein | 717 | 721 | A23 | Indomethacin inhibited IL-1 and NO production by rat microglia stimulated at the concentration of 0.1-10 micromol/l. | 694-817 | 694 | 817 | @SUBJECT$ @PREDICAT$ @OBJECT$ and NO production by rat microglia stimulated at the concentration of 0.1-10 micromol/l. |
Fact | preserve | 1128-1136 | 1128-1136 | T88 | increase | STIMULATES | 1,128 | 1,136 | preserve | 1202-1206 | 1202-1206 | T82 | DSCG | OrganicChemical | 1,202 | 1,206 | preserve | 1140-1150 | 1140-1150 | T78 | L-selectin | AminoAcidPeptideOrProtein | 1,140 | 1,150 | A1 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. | 973-1256 | 973 | 1,256 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an @PREDICAT$ of @OBJECT$ expression on monocytes after treatment with @SUBJECT$ , without any associated effect on CD11a and CD18. |
Fact | preserve | 1079-1081 | 1079-1081 | T86 | on | LOCATION_OF | 1,079 | 1,081 | preserve | 1082-1091 | 1082-1091 | T75 | monocytes | Cell | 1,082 | 1,091 | preserve | 1073-1078 | 1073-1078 | T74 | CD49d | AminoAcidPeptideOrProtein | 1,073 | 1,078 | A2 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. | 973-1256 | 973 | 1,256 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and @OBJECT$ @PREDICAT$ @SUBJECT$ and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. |
Fact | preserve | 1479-1483 | 1479-1483 | T108 | with | USES | 1,479 | 1,483 | preserve | 1469-1478 | 1469-1478 | T104 | treatment | TherapeuticOrPreventiveProcedure | 1,469 | 1,478 | preserve | 1484-1488 | 1484-1488 | T105 | DSCG | OrganicChemical | 1,484 | 1,488 | A3 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in asthmatic patients after the treatment with DSCG. | 1257-1489 | 1,257 | 1,489 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in asthmatic patients after the @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 509-511 | 509-511 | T36 | in | TREATS | 509 | 511 | preserve | 484-508 | 496-508 | T32 | therapeutic intervention | TherapeuticOrPreventiveProcedure | 484 | 508 | preserve | 527-535 | 527-535 | T34 | diseases | DiseaseOrSyndrome | 527 | 535 | A5 | Modulation of the expression of adhesion molecules may provide a potential new target for therapeutic intervention in allergic diseases. | 388-536 | 388 | 536 | Modulation of the expression of adhesion molecules may provide a potential new target for @SUBJECT$ @PREDICAT$ allergic @OBJECT$ . |
Uncommitted | preserve | 47-78 | 69-78 | T10 | disodium cromoglycate treatment | AFFECTS | 47 | 78 | preserve | 47-68 | 56-68 | T4 | disodium cromoglycate | OrganicChemical | 47 | 68 | preserve | 88-98 | 88-98 | T6 | asthmatics | DiseaseOrSyndrome | 88 | 98 | A7 | Expression of adhesion molecules and effect of disodium cromoglycate treatment in asthmatics. | 0-99 | 0 | 99 | Expression of adhesion molecules and effect of @SUBJECT$ @PREDICAT$ in @OBJECT$ . |
Fact | preserve | 870-872 | 870-872 | T65 | in | LOCATION_OF | 870 | 872 | preserve | 880-888 | 880-888 | T60 | patients | PatientOrDisabledGroup | 880 | 888 | preserve | 816-819 | 816-819 | T56 | IgE | GeneOrGenome | 816 | 819 | A8 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in atopic patients with mild asthma before and after treatment by disodium cromoglycate (DSCG). | 724-972 | 724 | 972 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for @OBJECT$ concentrations sCD23 were measured by ELISA @PREDICAT$ atopic @SUBJECT$ with mild asthma before and after treatment by disodium cromoglycate (DSCG). |
Uncommitted | preserve | 37-43 | 37-43 | T8 | effect | AFFECTS | 37 | 43 | preserve | 69-78 | 69-78 | T5 | treatment | TherapeuticOrPreventiveProcedure | 69 | 78 | preserve | 88-98 | 88-98 | T6 | asthmatics | DiseaseOrSyndrome | 88 | 98 | A12 | Expression of adhesion molecules and effect of disodium cromoglycate treatment in asthmatics. | 0-99 | 0 | 99 | Expression of adhesion molecules and @PREDICAT$ of disodium cromoglycate @SUBJECT$ in @OBJECT$ . |
Fact | preserve | 1434-1452 | 1444-1452 | T107 | asthmatic patients | PROCESS_OF | 1,434 | 1,452 | preserve | 1434-1443 | 1434-1443 | T102 | asthmatic | DiseaseOrSyndrome | 1,434 | 1,443 | preserve | 1444-1452 | 1444-1452 | T103 | patients | PatientOrDisabledGroup | 1,444 | 1,452 | A13 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in asthmatic patients after the treatment with DSCG. | 1257-1489 | 1,257 | 1,489 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in @SUBJECT$ @PREDICAT$ @OBJECT$ after the treatment with DSCG. |
Fact | preserve | 889-893 | 889-893 | T66 | with | PROCESS_OF | 889 | 893 | preserve | 894-905 | 899-905 | T61 | mild asthma | Finding | 894 | 905 | preserve | 880-888 | 880-888 | T60 | patients | PatientOrDisabledGroup | 880 | 888 | A14 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in atopic patients with mild asthma before and after treatment by disodium cromoglycate (DSCG). | 724-972 | 724 | 972 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in atopic @OBJECT$ @PREDICAT$ @SUBJECT$ before and after treatment by disodium cromoglycate (DSCG). |
Fact | preserve | 47-78 | 69-78 | T7 | disodium cromoglycate treatment | ISA | 47 | 78 | preserve | 47-68 | 56-68 | T4 | disodium cromoglycate | OrganicChemical | 47 | 68 | preserve | 69-78 | 69-78 | T5 | treatment | TherapeuticOrPreventiveProcedure | 69 | 78 | A15 | Expression of adhesion molecules and effect of disodium cromoglycate treatment in asthmatics. | 0-99 | 0 | 99 | Expression of adhesion molecules and effect of @SUBJECT$ @PREDICAT$ @OBJECT$ in asthmatics. |
Fact | preserve | 1079-1081 | 1079-1081 | T86 | on | LOCATION_OF | 1,079 | 1,081 | preserve | 1096-1107 | 1096-1107 | T76 | lymphocytes | Cell | 1,096 | 1,107 | preserve | 1073-1078 | 1073-1078 | T74 | CD49d | AminoAcidPeptideOrProtein | 1,073 | 1,078 | A16 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. | 973-1256 | 973 | 1,256 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and @OBJECT$ @PREDICAT$ monocytes and @SUBJECT$ as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. |
Fact | preserve | 47-78 | 69-78 | T9 | disodium cromoglycate treatment | USES | 47 | 78 | preserve | 69-78 | 69-78 | T5 | treatment | TherapeuticOrPreventiveProcedure | 69 | 78 | preserve | 47-68 | 56-68 | T4 | disodium cromoglycate | OrganicChemical | 47 | 68 | A17 | Expression of adhesion molecules and effect of disodium cromoglycate treatment in asthmatics. | 0-99 | 0 | 99 | Expression of adhesion molecules and effect of @OBJECT$ @PREDICAT$ @SUBJECT$ in asthmatics. |
Fact | preserve | 873-888 | 880-888 | T64 | atopic patients | PROCESS_OF | 873 | 888 | preserve | 873-879 | 873-879 | T59 | atopic | DiseaseOrSyndrome | 873 | 879 | preserve | 880-888 | 880-888 | T60 | patients | PatientOrDisabledGroup | 880 | 888 | A18 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in atopic patients with mild asthma before and after treatment by disodium cromoglycate (DSCG). | 724-972 | 724 | 972 | Serum concentrations of soluble ICAM-1, VCAM-1 and soluble low affinity receptor for IgE concentrations sCD23 were measured by ELISA in @SUBJECT$ @PREDICAT$ @OBJECT$ with mild asthma before and after treatment by disodium cromoglycate (DSCG). |
Fact | preserve | 1384-1388 | 1384-1388 | T106 | role | INTERACTS_WITH | 1,384 | 1,388 | preserve | 1348-1352 | 1348-1352 | T97 | CD23 | AminoAcidPeptideOrProtein | 1,348 | 1,352 | preserve | 1400-1403 | 1400-1403 | T100 | IgE | GeneOrGenome | 1,400 | 1,403 | A20 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble CD23 that plays a regulatory role in ongoing IgE production, were decreased in asthmatic patients after the treatment with DSCG. | 1257-1489 | 1,257 | 1,489 | The levels of soluble ICAM-1 and VCAM-1 were not changed, only the levels of soluble @SUBJECT$ that plays a regulatory @PREDICAT$ in ongoing @OBJECT$ production, were decreased in asthmatic patients after the treatment with DSCG. |
Fact | preserve | 1162-1164 | 1162-1164 | T89 | on | LOCATION_OF | 1,162 | 1,164 | preserve | 1165-1174 | 1165-1174 | T80 | monocytes | Cell | 1,165 | 1,174 | preserve | 1140-1150 | 1140-1150 | T78 | L-selectin | AminoAcidPeptideOrProtein | 1,140 | 1,150 | A21 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of L-selectin expression on monocytes after treatment with DSCG, without any associated effect on CD11a and CD18. | 973-1256 | 973 | 1,256 | The most significant finding was a significant decrease of ICAM-1 expression on monocytes and CD49d on monocytes and lymphocytes as well as an increase of @OBJECT$ expression @PREDICAT$ @SUBJECT$ after treatment with DSCG, without any associated effect on CD11a and CD18. |
Fact | preserve | 861-870 | 861-870 | T54 | treatment | TREATS | 861 | 870 | preserve | 840-852 | 840-852 | T49 | theophylline | BiologicallyActiveSubstance | 840 | 852 | preserve | 880-886 | 880-886 | T51 | asthma | DiseaseOrSyndrome | 880 | 886 | A2 | He was diagnosed as having the common cold with a bronchial asthmatic symptom and was prescribed 200 mg/day of sustained-release theophylline for the treatment of asthma for 7 days. | 699-898 | 699 | 898 | He was diagnosed as having the common cold with a bronchial asthmatic symptom and was prescribed 200 mg/day of sustained-release @SUBJECT$ for the @PREDICAT$ of @OBJECT$ for 7 days. |
Probable | preserve | 392-399 | 392-399 | T24 | treated | TREATS | 392 | 399 | preserve | 422-436 | 422-436 | T22 | clarithromycin | Antibiotic | 422 | 436 | preserve | 334-342 | 334-342 | T18 | Patients | PatientOrDisabledGroup | 334 | 342 | A3 | Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. | 334-450 | 334 | 450 | @OBJECT$ with upper respiratory infection are often @PREDICAT$ with theophylline and @SUBJECT$ concurrently. |
Fact | preserve | 497-503 | 497-500 | T34 | due to | CAUSES | 497 | 503 | preserve | 510-524 | 510-524 | T30 | rhabdomyolysis | PathologicFunction | 510 | 524 | preserve | 477-496 | 489-496 | T28 | acute renal failure | DiseaseOrSyndrome | 477 | 496 | A5 | We report a case of acute renal failure due to acute rhabdomyolysis caused by the interaction of theophylline and clarithromycin. | 451-592 | 451 | 592 | We report a case of @OBJECT$ @PREDICAT$ acute @SUBJECT$ caused by the interaction of theophylline and clarithromycin. |
Probable | preserve | 392-399 | 392-399 | T24 | treated | TREATS | 392 | 399 | preserve | 422-436 | 422-436 | T22 | clarithromycin | Antibiotic | 422 | 436 | preserve | 348-381 | 372-381 | T19 | upper respiratory infection | DiseaseOrSyndrome | 348 | 381 | A6 | Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. | 334-450 | 334 | 450 | Patients with @OBJECT$ are often @PREDICAT$ with theophylline and @SUBJECT$ concurrently. |
Fact | preserve | 343-347 | 343-347 | T23 | with | PROCESS_OF | 343 | 347 | preserve | 348-381 | 372-381 | T19 | upper respiratory infection | DiseaseOrSyndrome | 348 | 381 | preserve | 334-342 | 334-342 | T18 | Patients | PatientOrDisabledGroup | 334 | 342 | A7 | Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. | 334-450 | 334 | 450 | @OBJECT$ @PREDICAT$ @SUBJECT$ are often treated with theophylline and clarithromycin concurrently. |
Fact | preserve | 2154-2158 | 2154-2158 | T121 | with | PROCESS_OF | 2,154 | 2,158 | preserve | 2159-2170 | 2159-2170 | T120 | dehydration | DiseaseOrSyndrome | 2,159 | 2,170 | preserve | 2139-2147 | 2139-2147 | T119 | patients | PatientOrDisabledGroup | 2,139 | 2,147 | A8 | Theophylline toxicity may be enhanced when clarithromycin is administrated concomitantly, especially to elderly patients with dehydration. | 2021-2171 | 2,021 | 2,171 | Theophylline toxicity may be enhanced when clarithromycin is administrated concomitantly, especially to elderly @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 215-264 | 254-264 | T17 | Clarithromycin is a new oral macrolide antibiotic | ISA | 215 | 264 | preserve | 215-229 | 215-229 | T9 | Clarithromycin | Antibiotic | 215 | 229 | preserve | 244-264 | 254-264 | T12 | macrolide antibiotic | Antibiotic | 244 | 264 | A9 | Clarithromycin is a new oral macrolide antibiotic with excellent antibacterial activity and rare adverse effect. | 215-333 | 215 | 333 | @SUBJECT$ @PREDICAT$ @OBJECT$ with excellent antibacterial activity and rare adverse effect. |
Probable | preserve | 392-399 | 392-399 | T24 | treated | TREATS | 392 | 399 | preserve | 405-417 | 405-417 | T21 | theophylline | BiologicallyActiveSubstance | 405 | 417 | preserve | 334-342 | 334-342 | T18 | Patients | PatientOrDisabledGroup | 334 | 342 | A10 | Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. | 334-450 | 334 | 450 | @OBJECT$ with upper respiratory infection are often @PREDICAT$ with @SUBJECT$ and clarithromycin concurrently. |
Fact | preserve | 1894-1902 | 1894-1902 | T114 | enhances | STIMULATES | 1,894 | 1,902 | preserve | 1873-1887 | 1873-1887 | T108 | clarithromycin | Antibiotic | 1,873 | 1,887 | preserve | 1930-1942 | 1930-1942 | T110 | theophylline | BiologicallyActiveSubstance | 1,930 | 1,942 | A11 | It is well-known that clarithromycin enhances the serum concentration of theophylline by inhibition of the cytochrome P450-dependent pathway in hepatocytes. | 1851-2020 | 1,851 | 2,020 | It is well-known that @SUBJECT$ @PREDICAT$ the serum concentration of @OBJECT$ by inhibition of the cytochrome P450-dependent pathway in hepatocytes. |
Probable | preserve | 392-399 | 392-399 | T24 | treated | TREATS | 392 | 399 | preserve | 405-417 | 405-417 | T21 | theophylline | BiologicallyActiveSubstance | 405 | 417 | preserve | 348-381 | 372-381 | T19 | upper respiratory infection | DiseaseOrSyndrome | 348 | 381 | A12 | Patients with upper respiratory infection are often treated with theophylline and clarithromycin concurrently. | 334-450 | 334 | 450 | Patients with @OBJECT$ are often @PREDICAT$ with @SUBJECT$ and clarithromycin concurrently. |
Fact | preserve | 1398-1416 | 1408-1416 | T77 | asthmatic patients | PROCESS_OF | 1,398 | 1,416 | preserve | 1398-1407 | 1398-1407 | T75 | asthmatic | DiseaseOrSyndrome | 1,398 | 1,407 | preserve | 1408-1416 | 1408-1416 | T76 | patients | PatientOrDisabledGroup | 1,408 | 1,416 | A1 | The physiological role of beta-adrenergic receptors is unclear and their function seems normal in asthmatic patients. | 1294-1417 | 1,294 | 1,417 | The physiological role of beta-adrenergic receptors is unclear and their function seems normal in @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 1395-1397 | 1395-1397 | T78 | in | LOCATION_OF | 1,395 | 1,397 | preserve | 1408-1416 | 1408-1416 | T76 | patients | PatientOrDisabledGroup | 1,408 | 1,416 | preserve | 1320-1345 | 1336-1345 | T72 | beta-adrenergic receptors | AminoAcidPeptideOrProtein | 1,320 | 1,345 | A2 | The physiological role of beta-adrenergic receptors is unclear and their function seems normal in asthmatic patients. | 1294-1417 | 1,294 | 1,417 | The physiological role of @OBJECT$ is unclear and their function seems normal @PREDICAT$ asthmatic @SUBJECT$ . |
Doubtful | preserve | 943-945 | 943-945 | T57 | in | COEXISTS_WITH | 943 | 945 | preserve | 924-935 | 924-935 | T53 | dysfunction | PathologicFunction | 924 | 935 | preserve | 946-955 | 946-955 | T54 | asthmatic | DiseaseOrSyndrome | 946 | 955 | A6 | Although abnormalities of the cholinergic innervation have been suggested in asthma, thus far the evidence for cholinergic dysfunction in asthmatic subjects is not convincing. | 795-983 | 795 | 983 | Although abnormalities of the cholinergic innervation have been suggested in asthma, thus far the evidence for cholinergic @SUBJECT$ @PREDICAT$ @OBJECT$ subjects is not convincing. |
Fact | preserve | 312-330 | 322-330 | T26 | asthmatic patients | PROCESS_OF | 312 | 330 | preserve | 312-321 | 312-321 | T20 | asthmatic | DiseaseOrSyndrome | 312 | 321 | preserve | 322-330 | 322-330 | T21 | patients | PatientOrDisabledGroup | 322 | 330 | A7 | It has been suggested that neural control of the airways may be abnormal in asthmatic patients, and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. | 230-434 | 230 | 434 | It has been suggested that neural control of the airways may be abnormal in @SUBJECT$ @PREDICAT$ @OBJECT$ , and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. |
Fact | preserve | 88-90 | 88-90 | T8 | in | COEXISTS_WITH | 88 | 90 | preserve | 65-80 | 65-80 | T6 | pathophysiology | PathologicFunction | 65 | 80 | preserve | 91-97 | 91-97 | T7 | asthma | DiseaseOrSyndrome | 91 | 97 | A8 | Autonomic innervation of human airways: structure, function, and pathophysiology in asthma. | 0-98 | 0 | 98 | Autonomic innervation of human airways: structure, function, and @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 309-311 | 309-311 | T27 | in | PROCESS_OF | 309 | 311 | preserve | 257-277 | 270-277 | T17 | neural control | OrganOrTissueFunction | 257 | 277 | preserve | 322-330 | 322-330 | T21 | patients | PatientOrDisabledGroup | 322 | 330 | A9 | It has been suggested that neural control of the airways may be abnormal in asthmatic patients, and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. | 230-434 | 230 | 434 | It has been suggested that @SUBJECT$ of the airways may be abnormal @PREDICAT$ asthmatic @OBJECT$ , and that neurogenic mechanisms may contribute to the pathogenesis and pathophysiology of asthma. |
Fact | preserve | 771-793 | 781-793 | T47 | bronchial vasodilation | PROCESS_OF | 771 | 793 | preserve | 781-793 | 781-793 | T46 | vasodilation | PhysiologicFunction | 781 | 793 | preserve | 771-780 | 771-780 | T45 | bronchial | BodyPartOrganOrOrganComponent | 771 | 780 | A11 | Stimulation of cholinergic nerves causes bronchoconstriction, mucus secretion, and bronchial vasodilation. | 682-794 | 682 | 794 | Stimulation of cholinergic nerves causes bronchoconstriction, mucus secretion, and @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 1416-1423 | 1416-1423 | T87 | blocked | AFFECTS | 1,416 | 1,423 | preserve | 1427-1440 | 1427-1440 | T77 | cycloheximide | Antibiotic | 1,427 | 1,440 | preserve | 1399-1411 | 1399-1411 | T76 | upregulation | CellFunction | 1,399 | 1,411 | A1 | The upregulation was blocked by cycloheximide, indicating that it requires new protein synthesis, and was accompanied by an increase in both the stability of NK(2) receptor mRNA and the rate of NK(2) receptor gene transcription. | 1389-1635 | 1,389 | 1,635 | The @OBJECT$ was @PREDICAT$ by @SUBJECT$ , indicating that it requires new protein synthesis, and was accompanied by an increase in both the stability of NK(2) receptor mRNA and the rate of NK(2) receptor gene transcription. |
Fact | preserve | 2132-2138 | 2132-2138 | T120 | induce | CAUSES | 2,132 | 2,138 | preserve | 2123-2131 | 2123-2131 | T112 | agonists | PharmacologicSubstance | 2,123 | 2,131 | preserve | 2139-2151 | 2139-2151 | T113 | upregulation | CellFunction | 2,139 | 2,151 | A2 | We conclude that beta(2)-adrenoceptor agonists induce upregulation of functional NK(2) receptors in airway smooth muscle by increasing cAMP, and that this can be prevented by a corticosteroid. | 2079-2289 | 2,079 | 2,289 | We conclude that beta(2)-adrenoceptor @SUBJECT$ @PREDICAT$ @OBJECT$ of functional NK(2) receptors in airway smooth muscle by increasing cAMP, and that this can be prevented by a corticosteroid. |
Fact | preserve | 226-228 | 226-228 | T17 | in | LOCATION_OF | 226 | 228 | preserve | 229-236 | 229-236 | T13 | animals | Animal | 229 | 236 | preserve | 216-225 | 216-225 | T12 | receptors | AminoAcidPeptideOrProtein | 216 | 225 | A6 | Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK(2) receptors in animals and humans, and may be increased in asthma. | 134-280 | 134 | 280 | Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK(2) @OBJECT$ @PREDICAT$ @SUBJECT$ and humans, and may be increased in asthma. |
Fact | preserve | 153-160 | 153-160 | T16 | induces | AUGMENTS | 153 | 160 | preserve | 134-146 | 145-146 | T9 | Neurokinin A | AminoAcidPeptideOrProtein | 134 | 146 | preserve | 161-180 | 161-180 | T10 | bronchoconstriction | OrganOrTissueFunction | 161 | 180 | A7 | Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK(2) receptors in animals and humans, and may be increased in asthma. | 134-280 | 134 | 280 | @SUBJECT$ (NKA) @PREDICAT$ @OBJECT$ mediated by tachykinin NK(2) receptors in animals and humans, and may be increased in asthma. |
Fact | preserve | 226-228 | 226-228 | T17 | in | LOCATION_OF | 226 | 228 | preserve | 241-247 | 241-247 | T14 | humans | Human | 241 | 247 | preserve | 216-225 | 216-225 | T12 | receptors | AminoAcidPeptideOrProtein | 216 | 225 | A8 | Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK(2) receptors in animals and humans, and may be increased in asthma. | 134-280 | 134 | 280 | Neurokinin A (NKA) induces bronchoconstriction mediated by tachykinin NK(2) @OBJECT$ @PREDICAT$ animals and @SUBJECT$ , and may be increased in asthma. |
Fact | preserve | 2188-2190 | 2188-2190 | T121 | in | LOCATION_OF | 2,188 | 2,190 | preserve | 2198-2211 | 2205-2211 | T116 | smooth muscle | Tissue | 2,198 | 2,211 | preserve | 2172-2181 | 2172-2181 | T115 | receptors | AminoAcidPeptideOrProtein | 2,172 | 2,181 | A9 | We conclude that beta(2)-adrenoceptor agonists induce upregulation of functional NK(2) receptors in airway smooth muscle by increasing cAMP, and that this can be prevented by a corticosteroid. | 2079-2289 | 2,079 | 2,289 | We conclude that beta(2)-adrenoceptor agonists induce upregulation of functional NK(2) @OBJECT$ @PREDICAT$ airway @SUBJECT$ by increasing cAMP, and that this can be prevented by a corticosteroid. |
Fact | preserve | 366-368 | 366-368 | T48 | in | TREATS | 366 | 368 | preserve | 350-365 | 350-365 | T24 | bronchodilators | PharmacologicSubstance | 350 | 365 | preserve | 369-375 | 369-375 | T25 | asthma | DiseaseOrSyndrome | 369 | 375 | A10 | Because beta(2)-adrenoceptor agonists are the most widely used bronchodilators in asthma, we investigated the effects of the beta(2)-adrenoceptor agonist fenoterol on NK(2) receptor messenger RNA (mRNA) and receptor density as well as the functional responses of bovine tracheal smooth muscle to the NK(2) receptor agonist [beta-Ala(8)]-NKA(4-10) in vitro, using Northern blot analysis, receptor binding, and organ bath studies. | 281-746 | 281 | 746 | Because beta(2)-adrenoceptor agonists are the most widely used @SUBJECT$ @PREDICAT$ @OBJECT$ , we investigated the effects of the beta(2)-adrenoceptor agonist fenoterol on NK(2) receptor messenger RNA (mRNA) and receptor density as well as the functional responses of bovine tracheal smooth muscle to the NK(2) receptor agonist [beta-Ala(8)]-NKA(4-10) in vitro, using Northern blot analysis, receptor binding, and organ bath studies. |
Fact | preserve | 871-873 | 871-873 | T54 | in | PROCESS_OF | 871 | 873 | preserve | 832-846 | 838-846 | T50 | blood pressure | Finding | 832 | 846 | preserve | 878-885 | 878-885 | T53 | patient | PatientOrDisabledGroup | 878 | 885 | A1 | It confirmed the lack of hypertension, but the circadian rhythm of blood pressure was lost before surgery in one patient. | 758-886 | 758 | 886 | It confirmed the lack of hypertension, but the circadian rhythm of @SUBJECT$ was lost before surgery @PREDICAT$ one @OBJECT$ . |
Counterfact | preserve | 1340-1342 | 1340-1342 | T79 | in | PROCESS_OF | 1,340 | 1,342 | preserve | 1308-1326 | 1308-1326 | T76 | hyperaldosteronism | DiseaseOrSyndrome | 1,308 | 1,326 | preserve | 1348-1356 | 1348-1356 | T78 | patients | PatientOrDisabledGroup | 1,348 | 1,356 | A2 | Genetic screening for dexamethasone-sensitive hyperaldosteronism was negative in both patients. | 1256-1357 | 1,256 | 1,357 | Genetic screening for dexamethasone-sensitive @SUBJECT$ was negative @PREDICAT$ both @OBJECT$ . |
Counterfact | preserve | 331-334 | 331-334 | T29 | had | PROCESS_OF | 331 | 334 | preserve | 335-347 | 335-347 | T25 | hypertension | DiseaseOrSyndrome | 335 | 347 | preserve | 323-330 | 323-330 | T24 | patient | PatientOrDisabledGroup | 323 | 330 | A3 | Neither patient had hypertension, despite repeated measurements with a manual armlet. | 315-406 | 315 | 406 | Neither @OBJECT$ @PREDICAT$ @SUBJECT$ , despite repeated measurements with a manual armlet. |
Fact | preserve | 183-185 | 183-185 | T18 | in | PROCESS_OF | 183 | 185 | preserve | 174-182 | 174-182 | T12 | syndrome | DiseaseOrSyndrome | 174 | 182 | preserve | 202-207 | 202-207 | T15 | women | PopulationGroup | 202 | 207 | A4 | We report two new cases of this syndrome in two middle-aged women, one of Asian origin. | 136-229 | 136 | 229 | We report two new cases of this @SUBJECT$ @PREDICAT$ two middle-aged @OBJECT$ , one of Asian origin. |
Fact | preserve | 489-491 | 489-491 | T41 | in | PROCESS_OF | 489 | 491 | preserve | 439-465 | 447-465 | T31 | primary hyperaldosteronism | DiseaseOrSyndrome | 439 | 465 | preserve | 497-505 | 497-505 | T32 | patients | PatientOrDisabledGroup | 497 | 505 | A5 | A typical biological profile of primary hyperaldosteronism was demonstrated in both patients, including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. | 407-648 | 407 | 648 | A typical biological profile of @SUBJECT$ was demonstrated @PREDICAT$ both @OBJECT$ , including hypokalemia with inappropriate kaliuresis, elevated resting plasma aldosterone, and undetectable plasma renin activity. |
Fact | preserve | 815-819 | 815-819 | T47 | with | PROCESS_OF | 815 | 819 | preserve | 833-846 | 839-846 | T43 | heart failure | DiseaseOrSyndrome | 833 | 846 | preserve | 806-814 | 806-814 | T41 | patients | PatientOrDisabledGroup | 806 | 814 | A1 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | ACE inhibitors should be introduced with caution in @OBJECT$ @PREDICAT$ severe @SUBJECT$ and hypotension to prevent renal dysfunction. |
Uncommitted | preserve | 803-805 | 803-805 | T46 | in | TREATS | 803 | 805 | preserve | 754-768 | 758-768 | T40 | ACE inhibitors | PharmacologicSubstance | 754 | 768 | preserve | 833-846 | 839-846 | T43 | heart failure | DiseaseOrSyndrome | 833 | 846 | A2 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | @SUBJECT$ should be introduced with caution @PREDICAT$ patients with severe @OBJECT$ and hypotension to prevent renal dysfunction. |
Fact | preserve | 1052-1054 | 1052-1054 | T60 | in | PROCESS_OF | 1,052 | 1,054 | preserve | 1037-1051 | 1043-1051 | T55 | renal function | OrganOrTissueFunction | 1,037 | 1,051 | preserve | 1055-1063 | 1055-1063 | T56 | patients | PatientOrDisabledGroup | 1,055 | 1,063 | A3 | It also appears to have a neutral effect on renal function in patients with severe congestive heart failure. | 987-1107 | 987 | 1,107 | It also appears to have a neutral effect on @SUBJECT$ @PREDICAT$ @OBJECT$ with severe congestive heart failure. |
Uncommitted | preserve | 803-805 | 803-805 | T46 | in | TREATS | 803 | 805 | preserve | 754-768 | 758-768 | T40 | ACE inhibitors | PharmacologicSubstance | 754 | 768 | preserve | 806-814 | 806-814 | T41 | patients | PatientOrDisabledGroup | 806 | 814 | A5 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | @SUBJECT$ should be introduced with caution @PREDICAT$ @OBJECT$ with severe heart failure and hypotension to prevent renal dysfunction. |
Fact | preserve | 603-607 | 603-607 | T39 | with | USES | 603 | 607 | preserve | 593-602 | 593-602 | T28 | treatment | TherapeuticOrPreventiveProcedure | 593 | 602 | preserve | 608-622 | 612-622 | T29 | ACE inhibitors | PharmacologicSubstance | 608 | 622 | A6 | Skeletal muscle fatigue can play an important role in the pathophysiology of congestive heart failure, and only aggressive treatment with ACE inhibitors and exercise training can improve exercise tolerance and reduce the risk of further deterioration of cardiac function. | 457-753 | 457 | 753 | Skeletal muscle fatigue can play an important role in the pathophysiology of congestive heart failure, and only aggressive @SUBJECT$ @PREDICAT$ @OBJECT$ and exercise training can improve exercise tolerance and reduce the risk of further deterioration of cardiac function. |
Fact | preserve | 62-64 | 62-64 | T4 | in | COEXISTS_WITH | 62 | 64 | preserve | 45-61 | 55-61 | T2 | end-organ damage | DiseaseOrSyndrome | 45 | 61 | preserve | 65-78 | 71-78 | T3 | heart failure | DiseaseOrSyndrome | 65 | 78 | A8 | Angiotensin-converting enzyme inhibitors and end-organ damage in heart failure. | 0-79 | 0 | 79 | Angiotensin-converting enzyme inhibitors and @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 277-279 | 277-279 | T22 | in | TREATS | 277 | 279 | preserve | 262-276 | 266-276 | T12 | ACE inhibitors | PharmacologicSubstance | 262 | 276 | preserve | 280-304 | 297-304 | T13 | congestive heart failure | DiseaseOrSyndrome | 280 | 304 | A9 | The mechanisms of action of ACE inhibitors in congestive heart failure are multiple and may involve important effects on endothelial function in addition to the well known hemodynamic and neurohormonal effects. | 228-456 | 228 | 456 | The mechanisms of action of @SUBJECT$ @PREDICAT$ @OBJECT$ are multiple and may involve important effects on endothelial function in addition to the well known hemodynamic and neurohormonal effects. |
Fact | preserve | 815-819 | 815-819 | T47 | with | PROCESS_OF | 815 | 819 | preserve | 833-846 | 839-846 | T43 | heart failure | DiseaseOrSyndrome | 833 | 846 | preserve | 806-814 | 806-814 | T41 | patients | PatientOrDisabledGroup | 806 | 814 | A1 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | ACE inhibitors should be introduced with caution in @OBJECT$ @PREDICAT$ severe @SUBJECT$ and hypotension to prevent renal dysfunction. |
Fact | preserve | 803-805 | 803-805 | T46 | in | TREATS | 803 | 805 | preserve | 754-768 | 758-768 | T40 | ACE inhibitors | PharmacologicSubstance | 754 | 768 | preserve | 833-846 | 839-846 | T43 | heart failure | DiseaseOrSyndrome | 833 | 846 | A2 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | @SUBJECT$ should be introduced with caution @PREDICAT$ patients with severe @OBJECT$ and hypotension to prevent renal dysfunction. |
Fact | preserve | 1052-1054 | 1052-1054 | T60 | in | PROCESS_OF | 1,052 | 1,054 | preserve | 1037-1051 | 1043-1051 | T55 | renal function | OrganOrTissueFunction | 1,037 | 1,051 | preserve | 1055-1063 | 1055-1063 | T56 | patients | PatientOrDisabledGroup | 1,055 | 1,063 | A3 | It also appears to have a neutral effect on renal function in patients with severe congestive heart failure. | 987-1107 | 987 | 1,107 | It also appears to have a neutral effect on @SUBJECT$ @PREDICAT$ @OBJECT$ with severe congestive heart failure. |
Fact | preserve | 803-805 | 803-805 | T46 | in | TREATS | 803 | 805 | preserve | 754-768 | 758-768 | T40 | ACE inhibitors | PharmacologicSubstance | 754 | 768 | preserve | 806-814 | 806-814 | T41 | patients | PatientOrDisabledGroup | 806 | 814 | A5 | ACE inhibitors should be introduced with caution in patients with severe heart failure and hypotension to prevent renal dysfunction. | 754-892 | 754 | 892 | @SUBJECT$ should be introduced with caution @PREDICAT$ @OBJECT$ with severe heart failure and hypotension to prevent renal dysfunction. |
Fact | preserve | 603-607 | 603-607 | T39 | with | USES | 603 | 607 | preserve | 593-602 | 593-602 | T28 | treatment | TherapeuticOrPreventiveProcedure | 593 | 602 | preserve | 608-622 | 612-622 | T29 | ACE inhibitors | PharmacologicSubstance | 608 | 622 | A6 | Skeletal muscle fatigue can play an important role in the pathophysiology of congestive heart failure, and only aggressive treatment with ACE inhibitors and exercise training can improve exercise tolerance and reduce the risk of further deterioration of cardiac function. | 457-753 | 457 | 753 | Skeletal muscle fatigue can play an important role in the pathophysiology of congestive heart failure, and only aggressive @SUBJECT$ @PREDICAT$ @OBJECT$ and exercise training can improve exercise tolerance and reduce the risk of further deterioration of cardiac function. |