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Fact | preserve | 1469-1473 | 1469-1473 | T98 | with | USES | 1,469 | 1,473 | preserve | 1459-1468 | 1459-1468 | T93 | treatment | TherapeuticOrPreventiveProcedure | 1,459 | 1,468 | preserve | 1474-1484 | 1474-1484 | T94 | fosinopril | OrganophosphorusCompound | 1,474 | 1,484 | A21 | Serum levels of cVCAM-1 decreased by -19% (CI: -25% to -13%) after treatment with fosinopril (P = .003) and were no longer different from those of the control group. | 1385-1564 | 1,385 | 1,564 | Serum levels of cVCAM-1 decreased by -19% (CI: -25% to -13%) after @SUBJECT$ @PREDICAT$ @OBJECT$ (P = .003) and were no longer different from those of the control group. |
Fact | preserve | 1148-1150 | 1148-1150 | T75 | in | LOCATION_OF | 1,148 | 1,150 | preserve | 1151-1159 | 1151-1159 | T71 | patients | PatientOrDisabledGroup | 1,151 | 1,159 | preserve | 1106-1113 | 1106-1113 | T67 | cICAM-1 | AminoAcidPeptideOrProtein | 1,106 | 1,113 | A22 | As expected, baseline plasma concentrations of cE-selectin, cICAM-1, and cVCAM-1 were markedly higher in patients than in healthy control subjects (n = 82; P < .001). | 1040-1218 | 1,040 | 1,218 | As expected, baseline plasma concentrations of cE-selectin, @OBJECT$ , and cVCAM-1 were markedly higher @PREDICAT$ @SUBJECT$ than in healthy control subjects (n = 82; P < .001). |
Fact | preserve | 566-574 | 566-574 | T47 | received | ADMINISTERED_TO | 566 | 574 | preserve | 586-611 | 604-611 | T39 | intravenous heparin | Carbohydrate | 586 | 611 | preserve | 536-544 | 536-544 | T36 | patients | PatientOrDisabledGroup | 536 | 544 | A1 | METHODS: Thirteen patients with ulcerative colitis and four patients with Crohn's disease received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. | 470-676 | 470 | 676 | METHODS: Thirteen patients with ulcerative colitis and four @OBJECT$ with Crohn's disease @PREDICAT$ continuous @SUBJECT$ , aiming at a partial thromboplastin time of about 60 s for 2 wk. |
Fact | preserve | 1560-1576 | 1568-1576 | T98 | colonic bleeding | LOCATION_OF | 1,560 | 1,576 | preserve | 1560-1567 | 1560-1567 | T93 | colonic | BodyPartOrganOrOrganComponent | 1,560 | 1,567 | preserve | 1552-1576 | 1568-1576 | T94 | massive colonic bleeding | PathologicFunction | 1,552 | 1,576 | A2 | In one patient with ulcerative colitis, massive colonic bleeding was observed on day 11 of the study. | 1506-1613 | 1,506 | 1,613 | In one patient with ulcerative colitis, @OBJECT$ @SUBJECT$ @PREDICAT$ was observed on day 11 of the study. |
Fact | preserve | 545-549 | 545-549 | T45 | with | PROCESS_OF | 545 | 549 | preserve | 550-565 | 558-565 | T37 | Crohn's disease | DiseaseOrSyndrome | 550 | 565 | preserve | 536-544 | 536-544 | T36 | patients | PatientOrDisabledGroup | 536 | 544 | A3 | METHODS: Thirteen patients with ulcerative colitis and four patients with Crohn's disease received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. | 470-676 | 470 | 676 | METHODS: Thirteen patients with ulcerative colitis and four @OBJECT$ @PREDICAT$ @SUBJECT$ received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. |
Fact | preserve | 1521-1525 | 1521-1525 | T97 | with | PROCESS_OF | 1,521 | 1,525 | preserve | 1532-1550 | 1543-1550 | T92 | ulcerative colitis | DiseaseOrSyndrome | 1,532 | 1,550 | preserve | 1513-1520 | 1513-1520 | T91 | patient | PatientOrDisabledGroup | 1,513 | 1,520 | A4 | In one patient with ulcerative colitis, massive colonic bleeding was observed on day 11 of the study. | 1506-1613 | 1,506 | 1,613 | In one @OBJECT$ @PREDICAT$ @SUBJECT$ , massive colonic bleeding was observed on day 11 of the study. |
Fact | preserve | 382-384 | 382-384 | T29 | in | PROCESS_OF | 382 | 384 | preserve | 365-372 | 365-372 | T20 | disease | DiseaseOrSyndrome | 365 | 372 | preserve | 385-393 | 385-393 | T22 | patients | PatientOrDisabledGroup | 385 | 393 | A5 | This prospective study evaluated whether heparin results in improvement of disease activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. | 284-469 | 284 | 469 | This prospective study evaluated whether heparin results in improvement of @SUBJECT$ activity @PREDICAT$ @OBJECT$ with highly active, refractory ulcerative colitis or Crohn's disease. |
Fact | preserve | 1739-1743 | 1739-1743 | T108 | with | PROCESS_OF | 1,739 | 1,743 | preserve | 1758-1782 | 1775-1782 | T106 | ulcerative colitis | DiseaseOrSyndrome | 1,758 | 1,782 | preserve | 1730-1738 | 1730-1738 | T104 | patients | PatientOrDisabledGroup | 1,730 | 1,738 | A6 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned heparin in the therapy of patients with highly active ulcerative colitis. | 1614-1783 | 1,614 | 1,783 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned heparin in the therapy of @OBJECT$ @PREDICAT$ highly active @SUBJECT$ . |
Fact | preserve | 382-384 | 382-384 | T29 | in | PROCESS_OF | 382 | 384 | preserve | 453-468 | 461-468 | T26 | Crohn's disease | DiseaseOrSyndrome | 453 | 468 | preserve | 385-393 | 385-393 | T22 | patients | PatientOrDisabledGroup | 385 | 393 | A7 | This prospective study evaluated whether heparin results in improvement of disease activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. | 284-469 | 284 | 469 | This prospective study evaluated whether heparin results in improvement of disease activity @PREDICAT$ @OBJECT$ with highly active, refractory ulcerative colitis or @SUBJECT$ . |
Fact | preserve | 1125-1152 | 1144-1152 | T70 | ulcerative colitis patients | PROCESS_OF | 1,125 | 1,152 | preserve | 1125-1143 | 1136-1143 | T68 | ulcerative colitis | DiseaseOrSyndrome | 1,125 | 1,143 | preserve | 1144-1152 | 1144-1152 | T69 | patients | PatientOrDisabledGroup | 1,144 | 1,152 | A8 | RESULTS: A significant decline of clinical activity (p = 0.0059), C-reactive protein (p = 0.0119), and erythrocyte sedimentation rate (p = 0.0096) was observed in the ulcerative colitis patients. | 945-1153 | 945 | 1,153 | RESULTS: A significant decline of clinical activity (p = 0.0059), C-reactive protein (p = 0.0119), and erythrocyte sedimentation rate (p = 0.0096) was observed in the @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 497-501 | 497-501 | T43 | with | PROCESS_OF | 497 | 501 | preserve | 502-526 | 519-526 | T34 | ulcerative colitis | DiseaseOrSyndrome | 502 | 526 | preserve | 488-496 | 488-496 | T33 | patients | PatientOrDisabledGroup | 488 | 496 | A9 | METHODS: Thirteen patients with ulcerative colitis and four patients with Crohn's disease received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. | 470-676 | 470 | 676 | METHODS: Thirteen @OBJECT$ @PREDICAT$ @SUBJECT$ and four patients with Crohn's disease received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. |
Possible | preserve | 144-152 | 144-152 | T16 | improves | TREATS | 144 | 152 | preserve | 125-132 | 125-132 | T9 | heparin | BiologicallyActiveSubstance | 125 | 132 | preserve | 160-178 | 171-178 | T11 | ulcerative colitis | DiseaseOrSyndrome | 160 | 178 | A10 | OBJECTIVE: Unfractioned heparin reportedly improves severe ulcerative colitis and Crohn's disease, but most of the few observations made have been published as abstracts. | 101-283 | 101 | 283 | OBJECTIVE: Unfractioned @SUBJECT$ reportedly @PREDICAT$ severe @OBJECT$ and Crohn's disease, but most of the few observations made have been published as abstracts. |
Fact | preserve | 1118-1120 | 1118-1120 | T71 | in | PROCESS_OF | 1,118 | 1,120 | preserve | 1054-1084 | 1080-1084 | T67 | erythrocyte sedimentation rate | CellFunction | 1,054 | 1,084 | preserve | 1144-1152 | 1144-1152 | T69 | patients | PatientOrDisabledGroup | 1,144 | 1,152 | A11 | RESULTS: A significant decline of clinical activity (p = 0.0059), C-reactive protein (p = 0.0119), and erythrocyte sedimentation rate (p = 0.0096) was observed in the ulcerative colitis patients. | 945-1153 | 945 | 1,153 | RESULTS: A significant decline of clinical activity (p = 0.0059), C-reactive protein (p = 0.0119), and @SUBJECT$ (p = 0.0096) was observed @PREDICAT$ the ulcerative colitis @OBJECT$ . |
Uncommitted | preserve | 350-361 | 350-361 | T27 | improvement | TREATS | 350 | 361 | preserve | 325-332 | 325-332 | T19 | heparin | BiologicallyActiveSubstance | 325 | 332 | preserve | 453-468 | 461-468 | T26 | Crohn's disease | DiseaseOrSyndrome | 453 | 468 | A12 | This prospective study evaluated whether heparin results in improvement of disease activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. | 284-469 | 284 | 469 | This prospective study evaluated whether @SUBJECT$ results in @PREDICAT$ of disease activity in patients with highly active, refractory ulcerative colitis or @OBJECT$ . |
Uncommitted | preserve | 350-361 | 350-361 | T27 | improvement | TREATS | 350 | 361 | preserve | 325-332 | 325-332 | T19 | heparin | BiologicallyActiveSubstance | 325 | 332 | preserve | 365-372 | 365-372 | T20 | disease | DiseaseOrSyndrome | 365 | 372 | A13 | This prospective study evaluated whether heparin results in improvement of disease activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. | 284-469 | 284 | 469 | This prospective study evaluated whether @SUBJECT$ results in @PREDICAT$ of @OBJECT$ activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. |
Fact | preserve | 48-52 | 48-52 | T7 | with | PROCESS_OF | 48 | 52 | preserve | 67-99 | 92-99 | T5 | inflammatory bowel disease | DiseaseOrSyndrome | 67 | 99 | preserve | 39-47 | 39-47 | T3 | patients | PatientOrDisabledGroup | 39 | 47 | A14 | Unfractioned heparin in the therapy of patients with highly active inflammatory bowel disease. | 0-100 | 0 | 100 | Unfractioned heparin in the therapy of @OBJECT$ @PREDICAT$ highly active @SUBJECT$ . |
Fact | preserve | 1719-1726 | 1719-1726 | T107 | therapy | TREATS | 1,719 | 1,726 | preserve | 1704-1711 | 1704-1711 | T102 | heparin | BiologicallyActiveSubstance | 1,704 | 1,711 | preserve | 1730-1738 | 1730-1738 | T104 | patients | PatientOrDisabledGroup | 1,730 | 1,738 | A15 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned heparin in the therapy of patients with highly active ulcerative colitis. | 1614-1783 | 1,614 | 1,783 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned @SUBJECT$ in the @PREDICAT$ of @OBJECT$ with highly active ulcerative colitis. |
Fact | preserve | 1300-1324 | 1316-1324 | T85 | Crohn's disease patients | PROCESS_OF | 1,300 | 1,324 | preserve | 1300-1315 | 1308-1315 | T80 | Crohn's disease | DiseaseOrSyndrome | 1,300 | 1,315 | preserve | 1316-1324 | 1316-1324 | T81 | patients | PatientOrDisabledGroup | 1,316 | 1,324 | A16 | Seven patients with ulcerative colitis but none of the Crohn's disease patients achieved complete remission after an average of 4 wk. | 1239-1384 | 1,239 | 1,384 | Seven patients with ulcerative colitis but none of the @SUBJECT$ @PREDICAT$ @OBJECT$ achieved complete remission after an average of 4 wk. |
Fact | preserve | 28-35 | 28-35 | T6 | therapy | TREATS | 28 | 35 | preserve | 13-20 | 13-20 | T1 | heparin | BiologicallyActiveSubstance | 13 | 20 | preserve | 39-47 | 39-47 | T3 | patients | PatientOrDisabledGroup | 39 | 47 | A18 | Unfractioned heparin in the therapy of patients with highly active inflammatory bowel disease. | 0-100 | 0 | 100 | Unfractioned @SUBJECT$ in the @PREDICAT$ of @OBJECT$ with highly active inflammatory bowel disease. |
Fact | preserve | 28-35 | 28-35 | T6 | therapy | TREATS | 28 | 35 | preserve | 13-20 | 13-20 | T1 | heparin | BiologicallyActiveSubstance | 13 | 20 | preserve | 67-99 | 92-99 | T5 | inflammatory bowel disease | DiseaseOrSyndrome | 67 | 99 | A20 | Unfractioned heparin in the therapy of patients with highly active inflammatory bowel disease. | 0-100 | 0 | 100 | Unfractioned @SUBJECT$ in the @PREDICAT$ of patients with highly active @OBJECT$ . |
Fact | preserve | 1719-1726 | 1719-1726 | T107 | therapy | TREATS | 1,719 | 1,726 | preserve | 1704-1711 | 1704-1711 | T102 | heparin | BiologicallyActiveSubstance | 1,704 | 1,711 | preserve | 1758-1782 | 1775-1782 | T106 | ulcerative colitis | DiseaseOrSyndrome | 1,758 | 1,782 | A21 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned heparin in the therapy of patients with highly active ulcerative colitis. | 1614-1783 | 1,614 | 1,783 | CONCLUSIONS: These data are further evidence of a beneficial effect of unfractioned @SUBJECT$ in the @PREDICAT$ of patients with highly active @OBJECT$ . |
Possible | preserve | 1871-1873 | 1871-1873 | T115 | in | PROCESS_OF | 1,871 | 1,873 | preserve | 1812-1820 | 1812-1820 | T112 | bleeding | Finding | 1,812 | 1,820 | preserve | 1874-1895 | 1887-1895 | T114 | hospitalized patients | PatientOrDisabledGroup | 1,874 | 1,895 | A22 | Because of possible serious bleeding, intravenous heparin should be administered in hospitalized patients only. | 1784-1901 | 1,784 | 1,901 | Because of possible serious @SUBJECT$ , intravenous heparin should be administered @PREDICAT$ @OBJECT$ only. |
Fact | preserve | 394-398 | 394-398 | T31 | with | PROCESS_OF | 394 | 398 | preserve | 431-449 | 442-449 | T25 | ulcerative colitis | DiseaseOrSyndrome | 431 | 449 | preserve | 385-393 | 385-393 | T22 | patients | PatientOrDisabledGroup | 385 | 393 | A23 | This prospective study evaluated whether heparin results in improvement of disease activity in patients with highly active, refractory ulcerative colitis or Crohn's disease. | 284-469 | 284 | 469 | This prospective study evaluated whether heparin results in improvement of disease activity in @OBJECT$ @PREDICAT$ highly active, refractory @SUBJECT$ or Crohn's disease. |
Possible | preserve | 144-152 | 144-152 | T16 | improves | TREATS | 144 | 152 | preserve | 125-132 | 125-132 | T9 | heparin | BiologicallyActiveSubstance | 125 | 132 | preserve | 189-204 | 197-204 | T12 | Crohn's disease | DiseaseOrSyndrome | 189 | 204 | A24 | OBJECTIVE: Unfractioned heparin reportedly improves severe ulcerative colitis and Crohn's disease, but most of the few observations made have been published as abstracts. | 101-283 | 101 | 283 | OBJECTIVE: Unfractioned @SUBJECT$ reportedly @PREDICAT$ severe ulcerative colitis and @OBJECT$ , but most of the few observations made have been published as abstracts. |
Fact | preserve | 1254-1258 | 1254-1258 | T84 | with | PROCESS_OF | 1,254 | 1,258 | preserve | 1259-1283 | 1276-1283 | T79 | ulcerative colitis | DiseaseOrSyndrome | 1,259 | 1,283 | preserve | 1245-1253 | 1245-1253 | T78 | patients | PatientOrDisabledGroup | 1,245 | 1,253 | A25 | Seven patients with ulcerative colitis but none of the Crohn's disease patients achieved complete remission after an average of 4 wk. | 1239-1384 | 1,239 | 1,384 | Seven @OBJECT$ @PREDICAT$ @SUBJECT$ but none of the Crohn's disease patients achieved complete remission after an average of 4 wk. |
Fact | preserve | 566-574 | 566-574 | T47 | received | ADMINISTERED_TO | 566 | 574 | preserve | 586-611 | 604-611 | T39 | intravenous heparin | Carbohydrate | 586 | 611 | preserve | 488-496 | 488-496 | T33 | patients | PatientOrDisabledGroup | 488 | 496 | A26 | METHODS: Thirteen patients with ulcerative colitis and four patients with Crohn's disease received continuous intravenous heparin, aiming at a partial thromboplastin time of about 60 s for 2 wk. | 470-676 | 470 | 676 | METHODS: Thirteen @OBJECT$ with ulcerative colitis and four patients with Crohn's disease @PREDICAT$ continuous @SUBJECT$ , aiming at a partial thromboplastin time of about 60 s for 2 wk. |
Probable | preserve | 1216-1218 | 1216-1218 | T75 | in | TREATS | 1,216 | 1,218 | preserve | 1207-1215 | 1207-1215 | T67 | exercise | DailyOrRecreationalActivity | 1,207 | 1,215 | preserve | 1238-1254 | 1246-1254 | T69 | type II diabetes | DiseaseOrSyndrome | 1,238 | 1,254 | A1 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male patients with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. | 1101-1393 | 1,101 | 1,393 | These data show that serum leptin concentrations can be reduced with caloric restriction and @SUBJECT$ @PREDICAT$ male patients with @OBJECT$ , and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. |
Probable | preserve | 1216-1218 | 1216-1218 | T75 | in | TREATS | 1,216 | 1,218 | preserve | 1177-1196 | 1185-1196 | T66 | caloric restriction | TherapeuticOrPreventiveProcedure | 1,177 | 1,196 | preserve | 1224-1232 | 1224-1232 | T68 | patients | PatientOrDisabledGroup | 1,224 | 1,232 | A2 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male patients with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. | 1101-1393 | 1,101 | 1,393 | These data show that serum leptin concentrations can be reduced with @SUBJECT$ and exercise @PREDICAT$ male @OBJECT$ with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. |
Fact | preserve | 423-432 | 429-432 | T45 | obese men | PROCESS_OF | 423 | 432 | preserve | 423-428 | 423-428 | T29 | obese | DiseaseOrSyndrome | 423 | 428 | preserve | 429-432 | 429-432 | T30 | men | PopulationGroup | 429 | 432 | A3 | Twenty obese men (48 +/- 8 yr; body mass index 32. | 416-473 | 416 | 473 | Twenty @SUBJECT$ @PREDICAT$ @OBJECT$ (48 +/- 8 yr; body mass index 32. |
Fact | preserve | 493-497 | 493-497 | T46 | with | PROCESS_OF | 493 | 497 | preserve | 519-550 | 542-550 | T34 | type II diabetes mellitus | DiseaseOrSyndrome | 519 | 550 | preserve | 429-432 | 429-432 | T30 | men | PopulationGroup | 429 | 432 | A4 | 1 +/- 3.9 kg/m(2)) with previously diagnosed type II diabetes mellitus were assigned to a 4-wk intervention program of exercise (2, 200 kcal/wk) and diet (1,000 kcal/day; 50% carbohydrates, 25% protein, 25% fat; polyunsaturated-to-saturated fatty acid ratio 1.0). | 474-755 | 474 | 755 | 1 +/- 3.9 kg/m(2)) with previously diagnosed type II diabetes mellitus were assigned to a 4-wk intervention program of exercise (2, 200 kcal/wk) and diet (1,000 kcal/day; 50% carbohydrates, 25% protein, 25% fat; polyun @OBJECT$ @PREDICAT$ previously diagnosed @SUBJECT$ were assigned to a 4-wk intervention program of exercise (2, 200 kcal/wk) and diet (1,000 kcal/day; 50% carbohydrates, 25% protein, 25% fat; polyunsaturated-to-saturated fatty acid ratio 1.0). |
Fact | preserve | 88-92 | 88-92 | T12 | with | PROCESS_OF | 88 | 92 | preserve | 93-109 | 101-109 | T8 | type II diabetes | DiseaseOrSyndrome | 93 | 109 | preserve | 77-80 | 77-80 | T7 | men | PopulationGroup | 77 | 80 | A5 | Concurrent reductions of serum leptin and lipids during weight loss in obese men with type II diabetes. | 0-110 | 0 | 110 | Concurrent reductions of serum leptin and lipids during weight loss in obese @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 71-80 | 77-80 | T10 | obese men | PROCESS_OF | 71 | 80 | preserve | 71-76 | 71-76 | T6 | obese | DiseaseOrSyndrome | 71 | 76 | preserve | 77-80 | 77-80 | T7 | men | PopulationGroup | 77 | 80 | A9 | Concurrent reductions of serum leptin and lipids during weight loss in obese men with type II diabetes. | 0-110 | 0 | 110 | Concurrent reductions of serum leptin and lipids during weight loss in @SUBJECT$ @PREDICAT$ @OBJECT$ with type II diabetes. |
Probable | preserve | 1216-1218 | 1216-1218 | T75 | in | TREATS | 1,216 | 1,218 | preserve | 1207-1215 | 1207-1215 | T67 | exercise | DailyOrRecreationalActivity | 1,207 | 1,215 | preserve | 1224-1232 | 1224-1232 | T68 | patients | PatientOrDisabledGroup | 1,224 | 1,232 | A10 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male patients with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. | 1101-1393 | 1,101 | 1,393 | These data show that serum leptin concentrations can be reduced with caloric restriction and @SUBJECT$ @PREDICAT$ male @OBJECT$ with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. |
Fact | preserve | 25-37 | 31-37 | T9 | serum leptin | LOCATION_OF | 25 | 37 | preserve | 25-30 | 25-30 | T2 | serum | BodySubstance | 25 | 30 | preserve | 31-37 | 31-37 | T3 | leptin | AminoAcidPeptideOrProtein | 31 | 37 | A11 | Concurrent reductions of serum leptin and lipids during weight loss in obese men with type II diabetes. | 0-110 | 0 | 110 | Concurrent reductions of @SUBJECT$ @PREDICAT$ @OBJECT$ and lipids during weight loss in obese men with type II diabetes. |
Fact | preserve | 1233-1237 | 1233-1237 | T77 | with | PROCESS_OF | 1,233 | 1,237 | preserve | 1238-1254 | 1246-1254 | T69 | type II diabetes | DiseaseOrSyndrome | 1,238 | 1,254 | preserve | 1224-1232 | 1224-1232 | T68 | patients | PatientOrDisabledGroup | 1,224 | 1,232 | A12 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male patients with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. | 1101-1393 | 1,101 | 1,393 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male @OBJECT$ @PREDICAT$ @SUBJECT$ , and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. |
Fact | preserve | 68-70 | 68-70 | T11 | in | PROCESS_OF | 68 | 70 | preserve | 56-67 | 63-67 | T5 | weight loss | Finding | 56 | 67 | preserve | 77-80 | 77-80 | T7 | men | PopulationGroup | 77 | 80 | A13 | Concurrent reductions of serum leptin and lipids during weight loss in obese men with type II diabetes. | 0-110 | 0 | 110 | Concurrent reductions of serum leptin and lipids during @SUBJECT$ @PREDICAT$ obese @OBJECT$ with type II diabetes. |
Fact | preserve | 825-837 | 831-837 | T55 | serum leptin | LOCATION_OF | 825 | 837 | preserve | 825-830 | 825-830 | T50 | serum | BodySubstance | 825 | 830 | preserve | 831-837 | 831-837 | T51 | leptin | AminoAcidPeptideOrProtein | 831 | 837 | A14 | Intervention induced significant reductions in body weight and serum leptin levels, and improvements in lipoprotein profile and glucose control. | 756-912 | 756 | 912 | Intervention induced significant reductions in body weight and @SUBJECT$ @PREDICAT$ @OBJECT$ levels, and improvements in lipoprotein profile and glucose control. |
Fact | preserve | 227-229 | 227-229 | T26 | in | COEXISTS_WITH | 227 | 229 | preserve | 162-178 | 169-178 | T15 | weight reduction | Finding | 162 | 178 | preserve | 230-235 | 230-235 | T19 | obese | DiseaseOrSyndrome | 230 | 235 | A15 | The aim of the study was to examine the effects of weight reduction by exercise and diet on metabolic control in obese subjects with insulin resistance, particularly investigating if changes in serum leptin concentrations were directly associated with improvements in metabolic control. | 111-415 | 111 | 415 | The aim of the study was to examine the effects of @SUBJECT$ by exercise and diet on metabolic control @PREDICAT$ @OBJECT$ subjects with insulin resistance, particularly investigating if changes in serum leptin concentrations were directly associated with improvements in metabolic control. |
Probable | preserve | 1216-1218 | 1216-1218 | T75 | in | TREATS | 1,216 | 1,218 | preserve | 1177-1196 | 1185-1196 | T66 | caloric restriction | TherapeuticOrPreventiveProcedure | 1,177 | 1,196 | preserve | 1238-1254 | 1246-1254 | T69 | type II diabetes | DiseaseOrSyndrome | 1,238 | 1,254 | A16 | These data show that serum leptin concentrations can be reduced with caloric restriction and exercise in male patients with type II diabetes, and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. | 1101-1393 | 1,101 | 1,393 | These data show that serum leptin concentrations can be reduced with @SUBJECT$ and exercise @PREDICAT$ male patients with @OBJECT$ , and they suggest a direct relationship between leptin and lipoprotein metabolism that is not solely due to weight reduction. |
Fact | preserve | 606-610 | 606-610 | T42 | with | PROCESS_OF | 606 | 610 | preserve | 624-636 | 624-636 | T41 | hypertension | DiseaseOrSyndrome | 624 | 636 | preserve | 597-605 | 597-605 | T39 | patients | PatientOrDisabledGroup | 597 | 605 | A1 | There is also an urgent need to update existing guidelines and perhaps even provide specific guidelines for the treatment and long-term management of patients with diabetes and hypertension. | 435-637 | 435 | 637 | There is also an urgent need to update existing guidelines and perhaps even provide specific guidelines for the treatment and long-term management of @OBJECT$ @PREDICAT$ diabetes and @SUBJECT$ . |
Fact | preserve | 212-216 | 212-216 | T18 | with | PROCESS_OF | 212 | 216 | preserve | 236-248 | 236-248 | T15 | hypertension | DiseaseOrSyndrome | 236 | 248 | preserve | 203-211 | 203-211 | T13 | patients | PatientOrDisabledGroup | 203 | 211 | A2 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of patients with diabetes and hypertension. | 59-249 | 59 | 249 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of @OBJECT$ @PREDICAT$ diabetes and @SUBJECT$ . |
Fact | preserve | 606-610 | 606-610 | T42 | with | PROCESS_OF | 606 | 610 | preserve | 611-619 | 611-619 | T40 | diabetes | DiseaseOrSyndrome | 611 | 619 | preserve | 597-605 | 597-605 | T39 | patients | PatientOrDisabledGroup | 597 | 605 | A3 | There is also an urgent need to update existing guidelines and perhaps even provide specific guidelines for the treatment and long-term management of patients with diabetes and hypertension. | 435-637 | 435 | 637 | There is also an urgent need to update existing guidelines and perhaps even provide specific guidelines for the treatment and long-term management of @OBJECT$ @PREDICAT$ @SUBJECT$ and hypertension. |
Fact | preserve | 190-199 | 190-199 | T17 | treatment | TREATS | 190 | 199 | preserve | 147-168 | 159-168 | T10 | combination therapies | TherapeuticOrPreventiveProcedure | 147 | 168 | preserve | 236-248 | 236-248 | T15 | hypertension | DiseaseOrSyndrome | 236 | 248 | A4 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of patients with diabetes and hypertension. | 59-249 | 59 | 249 | In light of recent data from the UKPDS and HOT trials, it appears that intensive @SUBJECT$ are essential in the @PREDICAT$ of patients with diabetes and @OBJECT$ . |
Fact | preserve | 190-199 | 190-199 | T17 | treatment | TREATS | 190 | 199 | preserve | 147-168 | 159-168 | T10 | combination therapies | TherapeuticOrPreventiveProcedure | 147 | 168 | preserve | 203-211 | 203-211 | T13 | patients | PatientOrDisabledGroup | 203 | 211 | A5 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of patients with diabetes and hypertension. | 59-249 | 59 | 249 | In light of recent data from the UKPDS and HOT trials, it appears that intensive @SUBJECT$ are essential in the @PREDICAT$ of @OBJECT$ with diabetes and hypertension. |
Fact | preserve | 212-216 | 212-216 | T18 | with | PROCESS_OF | 212 | 216 | preserve | 217-225 | 217-225 | T14 | diabetes | DiseaseOrSyndrome | 217 | 225 | preserve | 203-211 | 203-211 | T13 | patients | PatientOrDisabledGroup | 203 | 211 | A7 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of patients with diabetes and hypertension. | 59-249 | 59 | 249 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of @OBJECT$ @PREDICAT$ @SUBJECT$ and hypertension. |
Fact | preserve | 190-199 | 190-199 | T17 | treatment | TREATS | 190 | 199 | preserve | 147-168 | 159-168 | T10 | combination therapies | TherapeuticOrPreventiveProcedure | 147 | 168 | preserve | 217-225 | 217-225 | T14 | diabetes | DiseaseOrSyndrome | 217 | 225 | A8 | In light of recent data from the UKPDS and HOT trials, it appears that intensive combination therapies are essential in the treatment of patients with diabetes and hypertension. | 59-249 | 59 | 249 | In light of recent data from the UKPDS and HOT trials, it appears that intensive @SUBJECT$ are essential in the @PREDICAT$ of patients with @OBJECT$ and hypertension. |
Possible | preserve | 1603-1614 | 1608-1614 | T85 | risk factor | PREDISPOSES | 1,603 | 1,614 | preserve | 1494-1503 | 1494-1503 | T75 | aldehydes | OrganicChemical | 1,494 | 1,503 | preserve | 1626-1645 | 1638-1645 | T82 | Alzheimer's disease | DiseaseOrSyndrome | 1,626 | 1,645 | A2 | Because the catalytic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protective effects of estrogen and generate aldehydes in neurons, it is proposed that a high concentration of this enzyme in brain is a potential risk factor for Alzheimer's disease. | 1328-1646 | 1,328 | 1,646 | Because the catalytic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protective effects of estrogen and generate @SUBJECT$ in neurons, it is proposed that a high concentration of this enzyme in brain is a potential @PREDICAT$ for @OBJECT$ . |
Fact | preserve | 469-471 | 469-471 | T31 | in | LOCATION_OF | 469 | 471 | preserve | 472-477 | 472-477 | T22 | cells | Cell | 472 | 477 | preserve | 455-468 | 455-468 | T21 | dehydrogenase | AminoAcidPeptideOrProtein | 455 | 468 | A3 | Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). | 364-638 | 364 | 638 | Mitochondria have been demonstrated to be the proper location of this NAD+-dependent @OBJECT$ @PREDICAT$ @SUBJECT$ , although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). |
Possible | preserve | 1504-1506 | 1504-1506 | T83 | in | LOCATION_OF | 1,504 | 1,506 | preserve | 1507-1514 | 1507-1514 | T76 | neurons | Cell | 1,507 | 1,514 | preserve | 1494-1503 | 1494-1503 | T75 | aldehydes | OrganicChemical | 1,494 | 1,503 | A4 | Because the catalytic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protective effects of estrogen and generate aldehydes in neurons, it is proposed that a high concentration of this enzyme in brain is a potential risk factor for Alzheimer's disease. | 1328-1646 | 1,328 | 1,646 | Because the catalytic functions of human brain short chain L-3-hydroxyacyl-CoA dehydrogenase could weaken the protective effects of estrogen and generate @OBJECT$ @PREDICAT$ @SUBJECT$ , it is proposed that a high concentration of this enzyme in brain is a potential risk factor for Alzheimer's disease. |
Fact | preserve | 1046-1055 | 1046-1055 | T56 | oxidation | INTERACTS_WITH | 1,046 | 1,055 | preserve | 1031-1037 | 1031-1037 | T50 | enzyme | Enzyme | 1,031 | 1,037 | preserve | 1066-1075 | 1066-1075 | T52 | estradiol | Hormone | 1,066 | 1,075 | A5 | The catalytic efficiency of this enzyme for the oxidation of 17beta-estradiol was comparable with that of peroxisomal 17beta-hydroxysteroid dehydrogenase type 4. | 992-1165 | 992 | 1,165 | The catalytic efficiency of this @SUBJECT$ for the @PREDICAT$ of 17beta- @OBJECT$ was comparable with that of peroxisomal 17beta-hydroxysteroid dehydrogenase type 4. |
Fact | preserve | 535-571 | 564-571 | T29 | amyloid beta-peptide binding protein | ISA | 535 | 571 | preserve | 535-555 | 543-555 | T25 | amyloid beta-peptide | AminoAcidPeptideOrProtein | 535 | 555 | preserve | 556-571 | 564-571 | T26 | binding protein | AminoAcidPeptideOrProtein | 556 | 571 | A6 | Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). | 364-638 | 364 | 638 | Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an @SUBJECT$ @PREDICAT$ @OBJECT$ reportedly associated with the endoplasmic reticulum (ERAB). |
Fact | preserve | 270-278 | 270-278 | T17 | catalyze | AFFECTS | 270 | 278 | preserve | 213-242 | 229-242 | T12 | hydroxyacyl-CoA dehydrogenase | DiseaseOrSyndrome | 213 | 242 | preserve | 283-292 | 283-292 | T14 | oxidation | PhenomenonOrProcess | 283 | 292 | A7 | Human brain short chain L-3-hydroxyacyl-CoA dehydrogenase (SCHAD) was found to catalyze the oxidation of 17beta-estradiol and dihydroandrosterone as well as alcohols. | 185-363 | 185 | 363 | Human brain short chain L-3- @SUBJECT$ (SCHAD) was found to @PREDICAT$ the @OBJECT$ of 17beta-estradiol and dihydroandrosterone as well as alcohols. |
Fact | preserve | 417-425 | 417-425 | T30 | location | LOCATION_OF | 417 | 425 | preserve | 364-376 | 364-376 | T18 | Mitochondria | CellComponent | 364 | 376 | preserve | 455-468 | 455-468 | T21 | dehydrogenase | AminoAcidPeptideOrProtein | 455 | 468 | A8 | Mitochondria have been demonstrated to be the proper location of this NAD+-dependent dehydrogenase in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). | 364-638 | 364 | 638 | @SUBJECT$ have been demonstrated to be the proper @PREDICAT$ of this NAD+-dependent @OBJECT$ in cells, although its primary structure is identical to an amyloid beta-peptide binding protein reportedly associated with the endoplasmic reticulum (ERAB). |
Fact | preserve | 745-756 | 745-756 | T38 | responsible | CAUSES | 745 | 756 | preserve | 709-744 | 731-744 | T35 | 17beta-hydroxysteroid dehydrogenase | AminoAcidPeptideOrProtein | 709 | 744 | preserve | 771-783 | 771-783 | T36 | inactivation | CellOrMolecularDysfunction | 771 | 783 | A9 | This fatty acid beta-oxidation enzyme was identified as a novel 17beta-hydroxysteroid dehydrogenase responsible for the inactivation of sex steroid hormones. | 639-808 | 639 | 808 | This fatty acid beta-oxidation enzyme was identified as a novel @SUBJECT$ @PREDICAT$ for the @OBJECT$ of sex steroid hormones. |
Fact | preserve | 494-504 | 494-504 | T30 | expression | PART_OF | 494 | 504 | preserve | 514-548 | 538-548 | T24 | cyclin-dependent kinase inhibitors | AminoAcidPeptideOrProtein | 514 | 548 | preserve | 563-577 | 572-577 | T26 | synovial cells | Cell | 563 | 577 | A2 | We studied the expression of cyclin-dependent kinase inhibitors in rheumatoid synovial cells as a means of suppressing synovial cell proliferation. | 479-638 | 479 | 638 | We studied the @PREDICAT$ of @SUBJECT$ in rheumatoid @OBJECT$ as a means of suppressing synovial cell proliferation. |
Fact | preserve | 86-95 | 86-95 | T9 | treatment | TREATS | 86 | 95 | preserve | 0-9 | 0-9 | T1 | Induction | TherapeuticOrPreventiveProcedure | 0 | 9 | preserve | 99-119 | 110-119 | T8 | rheumatoid arthritis | DiseaseOrSyndrome | 99 | 119 | A3 | Induction of the p16INK4a senescence gene as a new therapeutic strategy for the treatment of rheumatoid arthritis. | 0-120 | 0 | 120 | @SUBJECT$ of the p16INK4a senescence gene as a new therapeutic strategy for the @PREDICAT$ of @OBJECT$ . |
Fact | preserve | 994-996 | 994-996 | T48 | in | LOCATION_OF | 994 | 996 | preserve | 1000-1012 | 1007-1012 | T46 | animal model | Animal | 1,000 | 1,012 | preserve | 944-957 | 953-957 | T44 | p16INK4a gene | GeneOrGenome | 944 | 957 | A4 | In vivo adenoviral gene therapy with the p16INK4a gene efficiently inhibited the pathology in an animal model of rheumatoid arthritis. | 897-1043 | 897 | 1,043 | In vivo adenoviral gene therapy with the @OBJECT$ efficiently inhibited the pathology @PREDICAT$ an @SUBJECT$ of rheumatoid arthritis. |
Fact | preserve | 581-585 | 581-585 | T57 | with | PROCESS_OF | 581 | 585 | preserve | 595-608 | 602-608 | T41 | breast cancer | NeoplasticProcess | 595 | 608 | preserve | 572-580 | 572-580 | T40 | patients | PatientOrDisabledGroup | 572 | 580 | A2 | The objectives of this trial were (1) to gain experience with filgrastim given to patients with advanced breast cancer and receiving standard-dose CNF, and (2) to determine the maximum tolerated dose of CNF that could be given with filgrastim support by incremental dose escalation of two components of the CNF regimen, cyclophosphamide and mitoxantrone. | 483-862 | 483 | 862 | The objectives of this trial were (1) to gain experience with filgrastim given to @OBJECT$ @PREDICAT$ advanced @SUBJECT$ and receiving standard-dose CNF, and (2) to determine the maximum tolerated dose of CNF that could be given with filgrastim support by incremental dose escalation of two components of the CNF regimen, cyclophosphamide and mitoxantrone. |
Fact | preserve | 354-415 | 409-415 | T32 | human recombinant granulocyte-colony-stimulating factor | PART_OF | 354 | 415 | preserve | 360-415 | 409-415 | T26 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 360 | 415 | preserve | 354-359 | 354-359 | T25 | human | Human | 354 | 359 | A3 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. | 211-482 | 211 | 482 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with @OBJECT$ @PREDICAT$ @SUBJECT$ (G-CSF, filgrastim) in patients with advanced breast cancer. |
Fact | preserve | 436-438 | 436-438 | T33 | in | TREATS | 436 | 438 | preserve | 360-415 | 409-415 | T26 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 360 | 415 | preserve | 439-447 | 439-447 | T29 | patients | PatientOrDisabledGroup | 439 | 447 | A4 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. | 211-482 | 211 | 482 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human @SUBJECT$ (G-CSF, filgrastim) @PREDICAT$ @OBJECT$ with advanced breast cancer. |
Fact | preserve | 174-183 | 174-183 | T13 | treatment | TREATS | 174 | 183 | preserve | 137-149 | 137-149 | T7 | mitoxantrone | OrganicChemical | 137 | 149 | preserve | 196-209 | 203-209 | T10 | breast cancer | NeoplasticProcess | 196 | 209 | A6 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. | 0-210 | 0 | 210 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, @SUBJECT$ , and 5-FU in the @PREDICAT$ of advanced @OBJECT$ . |
Fact | preserve | 436-438 | 436-438 | T33 | in | TREATS | 436 | 438 | preserve | 360-415 | 409-415 | T26 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 360 | 415 | preserve | 468-481 | 475-481 | T30 | breast cancer | NeoplasticProcess | 468 | 481 | A7 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. | 211-482 | 211 | 482 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human @SUBJECT$ (G-CSF, filgrastim) @PREDICAT$ patients with advanced @OBJECT$ . |
Fact | preserve | 360-422 | 417-422 | T31 | recombinant granulocyte-colony-stimulating factor (G-CSF | ISA | 360 | 422 | preserve | 360-415 | 409-415 | T26 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 360 | 415 | preserve | 417-422 | 417-422 | T27 | G-CSF | AminoAcidPeptideOrProtein | 417 | 422 | A8 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. | 211-482 | 211 | 482 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human @SUBJECT$ @PREDICAT$ @OBJECT$ , filgrastim) in patients with advanced breast cancer. |
Fact | preserve | 20-75 | 69-75 | T12 | human recombinant granulocyte-colony-stimulating factor | PART_OF | 20 | 75 | preserve | 26-75 | 69-75 | T3 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 26 | 75 | preserve | 20-25 | 20-25 | T2 | human | Human | 20 | 25 | A10 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. | 0-210 | 0 | 210 | Phase I/II trial of @OBJECT$ @PREDICAT$ @SUBJECT$ (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. |
Fact | preserve | 563-568 | 563-568 | T56 | given | ADMINISTERED_TO | 563 | 568 | preserve | 552-562 | 552-562 | T39 | filgrastim | AminoAcidPeptideOrProtein | 552 | 562 | preserve | 572-580 | 572-580 | T40 | patients | PatientOrDisabledGroup | 572 | 580 | A11 | The objectives of this trial were (1) to gain experience with filgrastim given to patients with advanced breast cancer and receiving standard-dose CNF, and (2) to determine the maximum tolerated dose of CNF that could be given with filgrastim support by incremental dose escalation of two components of the CNF regimen, cyclophosphamide and mitoxantrone. | 483-862 | 483 | 862 | The objectives of this trial were (1) to gain experience with @SUBJECT$ @PREDICAT$ to @OBJECT$ with advanced breast cancer and receiving standard-dose CNF, and (2) to determine the maximum tolerated dose of CNF that could be given with filgrastim support by incremental dose escalation of two components of the CNF regimen, cyclophosphamide and mitoxantrone. |
Fact | preserve | 26-93 | 83-93 | T11 | recombinant granulocyte-colony-stimulating factor (filgrastim | ISA | 26 | 93 | preserve | 83-93 | 83-93 | T4 | filgrastim | AminoAcidPeptideOrProtein | 83 | 93 | preserve | 26-75 | 69-75 | T3 | recombinant granulocyte-colony-stimulating factor | AminoAcidPeptideOrProtein | 26 | 75 | A12 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. | 0-210 | 0 | 210 | Phase I/II trial of human @OBJECT$ @PREDICAT$ @SUBJECT$ ) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. |
Fact | preserve | 174-183 | 174-183 | T13 | treatment | TREATS | 174 | 183 | preserve | 155-159 | 155-159 | T8 | 5-FU | NucleicAcidNucleosideOrNucleotide | 155 | 159 | preserve | 196-209 | 203-209 | T10 | breast cancer | NeoplasticProcess | 196 | 209 | A14 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. | 0-210 | 0 | 210 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and @SUBJECT$ in the @PREDICAT$ of advanced @OBJECT$ . |
Fact | preserve | 448-452 | 448-452 | T34 | with | PROCESS_OF | 448 | 452 | preserve | 468-481 | 475-481 | T30 | breast cancer | NeoplasticProcess | 468 | 481 | preserve | 439-447 | 439-447 | T29 | patients | PatientOrDisabledGroup | 439 | 447 | A15 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in patients with advanced breast cancer. | 211-482 | 211 | 482 | PURPOSE: We performed a phase I/II dose-escalation trial of cyclophosphamide, mitoxantrone, and 5-fluorouracil (CNF) in combination with human recombinant granulocyte-colony-stimulating factor (G-CSF, filgrastim) in @OBJECT$ @PREDICAT$ advanced @SUBJECT$ . |
Fact | preserve | 174-183 | 174-183 | T13 | treatment | TREATS | 174 | 183 | preserve | 119-135 | 119-135 | T6 | cyclophosphamide | OrganophosphorusCompound | 119 | 135 | preserve | 196-209 | 203-209 | T10 | breast cancer | NeoplasticProcess | 196 | 209 | A16 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of cyclophosphamide, mitoxantrone, and 5-FU in the treatment of advanced breast cancer. | 0-210 | 0 | 210 | Phase I/II trial of human recombinant granulocyte-colony-stimulating factor (filgrastim) and escalating doses of @SUBJECT$ , mitoxantrone, and 5-FU in the @PREDICAT$ of advanced @OBJECT$ . |
Fact | preserve | 1843-1847 | 1843-1847 | T118 | with | PROCESS_OF | 1,843 | 1,847 | preserve | 1870-1888 | 1881-1888 | T114 | measurable disease | DiseaseOrSyndrome | 1,870 | 1,888 | preserve | 1834-1842 | 1834-1842 | T113 | patients | PatientOrDisabledGroup | 1,834 | 1,842 | A17 | Among 18 patients with bidimensionally measurable disease there were 3 complete (17%) and 5 partial (28%) responses. | 1825-1947 | 1,825 | 1,947 | Among 18 @OBJECT$ @PREDICAT$ bidimensionally @SUBJECT$ there were 3 complete (17%) and 5 partial (28%) responses. |
Fact | preserve | 1386-1395 | 1386-1395 | T85 | treatment | TREATS | 1,386 | 1,395 | preserve | 1361-1372 | 1361-1372 | T81 | leflunomide | OrganicChemical | 1,361 | 1,372 | preserve | 1399-1401 | 1399-1401 | T83 | RA | DiseaseOrSyndrome | 1,399 | 1,401 | A1 | CONCLUSIONS: The biochemical mechanisms underlying the therapeutic efficacy of low-dose methotrexate and leflunomide in the treatment of RA are quite different. | 1250-1422 | 1,250 | 1,422 | CONCLUSIONS: The biochemical mechanisms underlying the therapeutic efficacy of low-dose methotrexate and @SUBJECT$ in the @PREDICAT$ of @OBJECT$ are quite different. |
Fact | preserve | 691-693 | 691-693 | T46 | in | TREATS | 691 | 693 | preserve | 616-627 | 616-627 | T40 | leflunomide | OrganicChemical | 616 | 627 | preserve | 694-696 | 694-696 | T42 | RA | DiseaseOrSyndrome | 694 | 696 | A3 | This review compares the mode of action of methotrexate and leflunomide and speculates on how this contributes to therapeutic efficacy in RA when these agents are used singly or in combination. | 550-756 | 550 | 756 | This review compares the mode of action of methotrexate and @SUBJECT$ and speculates on how this contributes to therapeutic efficacy @PREDICAT$ @OBJECT$ when these agents are used singly or in combination. |
Fact | preserve | 691-693 | 691-693 | T46 | in | TREATS | 691 | 693 | preserve | 593-605 | 593-605 | T39 | methotrexate | OrganicChemical | 593 | 605 | preserve | 694-696 | 694-696 | T42 | RA | DiseaseOrSyndrome | 694 | 696 | A4 | This review compares the mode of action of methotrexate and leflunomide and speculates on how this contributes to therapeutic efficacy in RA when these agents are used singly or in combination. | 550-756 | 550 | 756 | This review compares the mode of action of @SUBJECT$ and leflunomide and speculates on how this contributes to therapeutic efficacy @PREDICAT$ @OBJECT$ when these agents are used singly or in combination. |
Fact | preserve | 1581-1584 | 1581-1584 | T98 | for | TREATS | 1,581 | 1,584 | preserve | 1561-1580 | 1573-1580 | T93 | combination therapy | TherapeuticOrPreventiveProcedure | 1,561 | 1,580 | preserve | 1585-1593 | 1585-1593 | T94 | patients | PatientOrDisabledGroup | 1,585 | 1,593 | A5 | The potentially complementary mechanisms of action of these two effective DMARDs should provide a rationale for their use in combination therapy for patients whose condition no longer responds to methotrexate alone. | 1423-1657 | 1,423 | 1,657 | The potentially complementary mechanisms of action of these two effective DMARDs should provide a rationale for their use in @SUBJECT$ @PREDICAT$ @OBJECT$ whose condition no longer responds to methotrexate alone. |
Fact | preserve | 253-262 | 253-262 | T20 | treatment | TREATS | 253 | 262 | preserve | 198-235 | 230-235 | T16 | disease-modifying antirheumatic drugs | PharmacologicSubstance | 198 | 235 | preserve | 266-292 | 283-292 | T18 | rheumatoid arthritis | DiseaseOrSyndrome | 266 | 292 | A6 | OBJECTIVES: Methotrexate is currently one of the most widely prescribed disease-modifying antirheumatic drugs (DMARDs) for the treatment of rheumatoid arthritis (RA). | 120-298 | 120 | 298 | OBJECTIVES: Methotrexate is currently one of the most widely prescribed @SUBJECT$ (DMARDs) for the @PREDICAT$ of @OBJECT$ (RA). |
Fact | preserve | 916-918 | 916-918 | T57 | in | TREATS | 916 | 918 | preserve | 887-899 | 887-899 | T53 | methotrexate | OrganicChemical | 887 | 899 | preserve | 928-930 | 928-930 | T56 | RA | DiseaseOrSyndrome | 928 | 930 | A7 | METHODS: A literature review of the biochemical mechanisms considered to be the basis for the therapeutic efficacy of methotrexate and leflunomide in treating RA is presented. | 757-944 | 757 | 944 | METHODS: A literature review of the biochemical mechanisms considered to be the basis for the therapeutic efficacy of @SUBJECT$ and leflunomide @PREDICAT$ treating @OBJECT$ is presented. |
Fact | preserve | 562-570 | 562-570 | T45 | compares | compared_with | 562 | 570 | preserve | 593-605 | 593-605 | T39 | methotrexate | OrganicChemical | 593 | 605 | preserve | 616-627 | 616-627 | T40 | leflunomide | OrganicChemical | 616 | 627 | A8 | This review compares the mode of action of methotrexate and leflunomide and speculates on how this contributes to therapeutic efficacy in RA when these agents are used singly or in combination. | 550-756 | 550 | 756 | This review @PREDICAT$ the mode of action of @SUBJECT$ and @OBJECT$ and speculates on how this contributes to therapeutic efficacy in RA when these agents are used singly or in combination. |
Fact | preserve | 525-529 | 525-529 | T37 | with | USES | 525 | 529 | preserve | 505-524 | 517-524 | T35 | combination therapy | TherapeuticOrPreventiveProcedure | 505 | 524 | preserve | 536-548 | 536-548 | T36 | methotrexate | OrganicChemical | 536 | 548 | A9 | Leflunomide is a new DMARD that may have a high potential for success in combination therapy with methotrexate. | 426-549 | 426 | 549 | Leflunomide is a new DMARD that may have a high potential for success in @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 48-51 | 48-51 | T8 | for | USES | 48 | 51 | preserve | 52-71 | 64-71 | T5 | combination therapy | TherapeuticOrPreventiveProcedure | 52 | 71 | preserve | 0-12 | 0-12 | T1 | Methotrexate | OrganicChemical | 0 | 12 | A10 | Methotrexate and leflunomide: biochemical basis for combination therapy in the treatment of rheumatoid arthritis. | 0-119 | 0 | 119 | @OBJECT$ and leflunomide: biochemical basis @PREDICAT$ @SUBJECT$ in the treatment of rheumatoid arthritis. |
Fact | preserve | 982-990 | 982-990 | T69 | inhibits | DISRUPTS | 982 | 990 | preserve | 969-981 | 969-981 | T61 | methotrexate | OrganicChemical | 969 | 981 | preserve | 991-1010 | 1000-1010 | T62 | cytokine production | MolecularFunction | 991 | 1,010 | A11 | RESULTS: Low-dose methotrexate inhibits cytokine production, purine biosynthesis, and, in an animal model, causes the release of adenosine, a potent antiinflammatory agent. | 945-1136 | 945 | 1,136 | RESULTS: Low-dose @SUBJECT$ @PREDICAT$ @OBJECT$ , purine biosynthesis, and, in an animal model, causes the release of adenosine, a potent antiinflammatory agent. |
Fact | preserve | 48-51 | 48-51 | T8 | for | USES | 48 | 51 | preserve | 52-71 | 64-71 | T5 | combination therapy | TherapeuticOrPreventiveProcedure | 52 | 71 | preserve | 17-28 | 17-28 | T2 | leflunomide | OrganicChemical | 17 | 28 | A12 | Methotrexate and leflunomide: biochemical basis for combination therapy in the treatment of rheumatoid arthritis. | 0-119 | 0 | 119 | Methotrexate and @OBJECT$ : biochemical basis @PREDICAT$ @SUBJECT$ in the treatment of rheumatoid arthritis. |
Fact | preserve | 1158-1168 | 1158-1168 | T76 | inhibition | INHIBITS | 1,158 | 1,168 | preserve | 1137-1148 | 1137-1148 | T71 | Leflunomide | OrganicChemical | 1,137 | 1,148 | preserve | 1180-1190 | 1180-1190 | T73 | pyrimidine | OrganicChemical | 1,180 | 1,190 | A13 | Leflunomide, through inhibition of de novo pyrimidine biosynthesis, can regulate lymphocyte proliferation. | 1137-1249 | 1,137 | 1,249 | @SUBJECT$ , through @PREDICAT$ of de novo @OBJECT$ biosynthesis, can regulate lymphocyte proliferation. |
Fact | preserve | 132-262 | 148-157 | T19 | Methotrexate is currently one of the most widely prescribed disease-modifying antirheumatic drugs (DMARDs) for the treatment | ISA | 132 | 262 | preserve | 132-144 | 132-144 | T11 | Methotrexate | OrganicChemical | 132 | 144 | preserve | 253-262 | 253-262 | T17 | treatment | TherapeuticOrPreventiveProcedure | 253 | 262 | A14 | OBJECTIVES: Methotrexate is currently one of the most widely prescribed disease-modifying antirheumatic drugs (DMARDs) for the treatment of rheumatoid arthritis (RA). | 120-298 | 120 | 298 | OBJECTIVES: @SUBJECT$ @PREDICAT$ @OBJECT$ of rheumatoid arthritis (RA). |
Fact | preserve | 916-918 | 916-918 | T57 | in | TREATS | 916 | 918 | preserve | 904-915 | 904-915 | T54 | leflunomide | OrganicChemical | 904 | 915 | preserve | 928-930 | 928-930 | T56 | RA | DiseaseOrSyndrome | 928 | 930 | A15 | METHODS: A literature review of the biochemical mechanisms considered to be the basis for the therapeutic efficacy of methotrexate and leflunomide in treating RA is presented. | 757-944 | 757 | 944 | METHODS: A literature review of the biochemical mechanisms considered to be the basis for the therapeutic efficacy of methotrexate and @SUBJECT$ @PREDICAT$ treating @OBJECT$ is presented. |
Fact | preserve | 335-339 | 335-339 | T28 | with | USES | 335 | 339 | preserve | 299-318 | 311-318 | T21 | Combination therapy | TherapeuticOrPreventiveProcedure | 299 | 318 | preserve | 346-352 | 346-352 | T23 | DMARDs | PharmacologicSubstance | 346 | 352 | A16 | Combination therapy of methotrexate with other DMARDs increases the clinical success of low-dose methotrexate treatment. | 299-425 | 299 | 425 | @SUBJECT$ of methotrexate @PREDICAT$ other @OBJECT$ increases the clinical success of low-dose methotrexate treatment. |
Fact | preserve | 1386-1395 | 1386-1395 | T85 | treatment | TREATS | 1,386 | 1,395 | preserve | 1344-1356 | 1344-1356 | T80 | methotrexate | OrganicChemical | 1,344 | 1,356 | preserve | 1399-1401 | 1399-1401 | T83 | RA | DiseaseOrSyndrome | 1,399 | 1,401 | A17 | CONCLUSIONS: The biochemical mechanisms underlying the therapeutic efficacy of low-dose methotrexate and leflunomide in the treatment of RA are quite different. | 1250-1422 | 1,250 | 1,422 | CONCLUSIONS: The biochemical mechanisms underlying the therapeutic efficacy of low-dose @SUBJECT$ and leflunomide in the @PREDICAT$ of @OBJECT$ are quite different. |
Fact | preserve | 983-987 | 983-987 | T63 | with | PROCESS_OF | 983 | 987 | preserve | 988-992 | 988-992 | T58 | IDDM | DiseaseOrSyndrome | 988 | 992 | preserve | 974-982 | 974-982 | T57 | patients | PatientOrDisabledGroup | 974 | 982 | A4 | digoxin-like factor was detected in 90% of patients with IDDM, and it can be used as a risk factor of the occurrence of vascular complications. | 925-1080 | 925 | 1,080 | digoxin-like factor was detected in 90% of @OBJECT$ @PREDICAT$ @SUBJECT$ , and it can be used as a risk factor of the occurrence of vascular complications. |
Probable | preserve | 1018-1029 | 1023-1029 | T64 | risk factor | PREDISPOSES | 1,018 | 1,029 | preserve | 925-932 | 925-932 | T54 | digoxin | Carbohydrate | 925 | 932 | preserve | 1066-1079 | 1066-1079 | T62 | complications | PathologicFunction | 1,066 | 1,079 | A5 | digoxin-like factor was detected in 90% of patients with IDDM, and it can be used as a risk factor of the occurrence of vascular complications. | 925-1080 | 925 | 1,080 | @SUBJECT$ -like factor was detected in 90% of patients with IDDM, and it can be used as a @PREDICAT$ of the occurrence of vascular @OBJECT$ . |
Fact | preserve | 1641-1643 | 1641-1643 | T104 | in | LOCATION_OF | 1,641 | 1,643 | preserve | 1648-1653 | 1648-1653 | T99 | blood | Tissue | 1,648 | 1,653 | preserve | 1591-1603 | 1591-1603 | T96 | theophylline | BiologicallyActiveSubstance | 1,591 | 1,603 | A6 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and phenytoin-like substances in the blood of the healthy people who did not receive any drugs. | 1509-1706 | 1,509 | 1,706 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, @OBJECT$ - and phenytoin-like substances @PREDICAT$ the @SUBJECT$ of the healthy people who did not receive any drugs. |
Fact | preserve | 293-295 | 293-295 | T26 | in | LOCATION_OF | 293 | 295 | preserve | 300-308 | 300-308 | T18 | organism | Organism | 300 | 308 | preserve | 258-266 | 258-266 | T15 | receptor | AminoAcidPeptideOrProtein | 258 | 266 | A7 | endorphin and enkephalin, is one of the most spectacular indications suggesting that the presence of a receptor for a certain drug in the organism authenticates searching for an endogenous substances with high affinity at this receptor. | 149-404 | 149 | 404 | endorphin and enkephalin, is one of the most spectacular indications suggesting that the presence of a @OBJECT$ for a certain drug @PREDICAT$ the @SUBJECT$ authenticates searching for an endogenous substances with high affinity at this receptor. |
Fact | preserve | 1641-1643 | 1641-1643 | T104 | in | LOCATION_OF | 1,641 | 1,643 | preserve | 1648-1653 | 1648-1653 | T99 | blood | Tissue | 1,648 | 1,653 | preserve | 1577-1588 | 1577-1588 | T95 | cyclosporin | AminoAcidPeptideOrProtein | 1,577 | 1,588 | A9 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and phenytoin-like substances in the blood of the healthy people who did not receive any drugs. | 1509-1706 | 1,509 | 1,706 | In our studies we ascertained the presence of the quinidine-, @OBJECT$ -, theophylline- and phenytoin-like substances @PREDICAT$ the @SUBJECT$ of the healthy people who did not receive any drugs. |
Fact | preserve | 788-803 | 793-803 | T50 | drug treatments | USES | 788 | 803 | preserve | 793-803 | 793-803 | T48 | treatments | TherapeuticOrPreventiveProcedure | 793 | 803 | preserve | 788-792 | 788-792 | T47 | drug | PharmacologicSubstance | 788 | 792 | A10 | Digoxin-like factor was detected in blood of healthy people who did not receive any drug treatments. | 698-804 | 698 | 804 | Digoxin-like factor was detected in blood of healthy people who did not receive any @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 731-733 | 731-733 | T49 | in | LOCATION_OF | 731 | 733 | preserve | 734-739 | 734-739 | T43 | blood | Tissue | 734 | 739 | preserve | 698-705 | 698-705 | T41 | Digoxin | Carbohydrate | 698 | 705 | A11 | Digoxin-like factor was detected in blood of healthy people who did not receive any drug treatments. | 698-804 | 698 | 804 | @OBJECT$ -like factor was detected @PREDICAT$ @SUBJECT$ of healthy people who did not receive any drug treatments. |
Fact | preserve | 1791-1812 | 1804-1812 | T116 | human organism | ISA | 1,791 | 1,812 | preserve | 1791-1796 | 1791-1796 | T111 | human | Human | 1,791 | 1,796 | preserve | 1804-1812 | 1804-1812 | T112 | organism | Organism | 1,804 | 1,812 | A13 | It seems that these endogenous substances resembling drugs are synthesized in human organism when they are needed for maintaining the physiological equilibrium. | 1707-1880 | 1,707 | 1,880 | It seems that these endogenous substances resembling drugs are synthesized in @SUBJECT$ @PREDICAT$ @OBJECT$ when they are needed for maintaining the physiological equilibrium. |
Fact | preserve | 1157-1161 | 1157-1161 | T73 | with | PROCESS_OF | 1,157 | 1,161 | preserve | 1162-1180 | 1162-1180 | T71 | insulin-resistance | PathologicFunction | 1,162 | 1,180 | preserve | 1148-1156 | 1148-1156 | T70 | patients | PatientOrDisabledGroup | 1,148 | 1,156 | A14 | In cases with NIDDM, the digoxin-like factor was detected in patients with insulin-resistance. | 1081-1181 | 1,081 | 1,181 | In cases with NIDDM, the digoxin-like factor was detected in @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 1252-1256 | 1252-1256 | T81 | with | PROCESS_OF | 1,252 | 1,256 | preserve | 1257-1270 | 1263-1270 | T77 | heart failure | DiseaseOrSyndrome | 1,257 | 1,270 | preserve | 1243-1251 | 1243-1251 | T76 | patients | PatientOrDisabledGroup | 1,243 | 1,251 | A16 | The presence of digoxin-like factor was ascertained in patients with heart failure who did not take digitalis preparations. | 1182-1317 | 1,182 | 1,317 | The presence of digoxin-like factor was ascertained in @OBJECT$ @PREDICAT$ @SUBJECT$ who did not take digitalis preparations. |
Fact | preserve | 1057-1079 | 1066-1079 | T65 | vascular complications | LOCATION_OF | 1,057 | 1,079 | preserve | 1057-1065 | 1057-1065 | T61 | vascular | BodyPartOrganOrOrganComponent | 1,057 | 1,065 | preserve | 1066-1079 | 1066-1079 | T62 | complications | PathologicFunction | 1,066 | 1,079 | A18 | digoxin-like factor was detected in 90% of patients with IDDM, and it can be used as a risk factor of the occurrence of vascular complications. | 925-1080 | 925 | 1,080 | digoxin-like factor was detected in 90% of patients with IDDM, and it can be used as a risk factor of the occurrence of @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 1641-1643 | 1641-1643 | T104 | in | LOCATION_OF | 1,641 | 1,643 | preserve | 1648-1653 | 1648-1653 | T99 | blood | Tissue | 1,648 | 1,653 | preserve | 1565-1574 | 1565-1574 | T94 | quinidine | BiologicallyActiveSubstance | 1,565 | 1,574 | A20 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and phenytoin-like substances in the blood of the healthy people who did not receive any drugs. | 1509-1706 | 1,509 | 1,706 | In our studies we ascertained the presence of the @OBJECT$ -, cyclosporin-, theophylline- and phenytoin-like substances @PREDICAT$ the @SUBJECT$ of the healthy people who did not receive any drugs. |
Fact | preserve | 1641-1643 | 1641-1643 | T104 | in | LOCATION_OF | 1,641 | 1,643 | preserve | 1648-1653 | 1648-1653 | T99 | blood | Tissue | 1,648 | 1,653 | preserve | 1609-1618 | 1609-1618 | T97 | phenytoin | OrganicChemical | 1,609 | 1,618 | A21 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and phenytoin-like substances in the blood of the healthy people who did not receive any drugs. | 1509-1706 | 1,509 | 1,706 | In our studies we ascertained the presence of the quinidine-, cyclosporin-, theophylline- and @OBJECT$ -like substances @PREDICAT$ the @SUBJECT$ of the healthy people who did not receive any drugs. |
Counterfact | preserve | 1161-1167 | 1161-1167 | T80 | affect | INTERACTS_WITH | 1,161 | 1,167 | preserve | 1046-1056 | 1046-1056 | T70 | amlodipine | OrganicChemical | 1,046 | 1,056 | preserve | 1168-1171 | 1168-1171 | T76 | Ca2 | GeneOrGenome | 1,168 | 1,171 | A1 | Within its effective pharmacological range (10-100 nM), amlodipine attenuated intracellular neuronal Ca2+ increases elicited by KCl depolarization but did not affect Ca2+ changes triggered by N-methyl-D-aspartate receptor activation. | 990-1241 | 990 | 1,241 | Within its effective pharmacological range (10-100 nM), @SUBJECT$ attenuated intracellular neuronal Ca2+ increases elicited by KCl depolarization but did not @PREDICAT$ @OBJECT$ + changes triggered by N-methyl-D-aspartate receptor activation. |