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Fact | preserve | 956-959 | 956-959 | T55 | had | PROCESS_OF | 956 | 959 | preserve | 960-991 | 982-991 | T54 | intra-abdominal abscesses | DiseaseOrSyndrome | 960 | 991 | preserve | 909-917 | 909-917 | T51 | patients | PatientOrDisabledGroup | 909 | 917 | A6 | Two patients with laparoscopic ileocolic resection had intra-abdominal abscesses, which were drained percutaneously in both. | 905-1035 | 905 | 1,035 | Two @OBJECT$ with laparoscopic ileocolic resection @PREDICAT$ @SUBJECT$ , which were drained percutaneously in both. |
Fact | preserve | 181-183 | 181-183 | T15 | in | TREATS | 181 | 183 | preserve | 140-166 | 159-166 | T11 | Laparoscopic bowel surgery | TherapeuticOrPreventiveProcedure | 140 | 166 | preserve | 199-207 | 199-207 | T12 | patients | PatientOrDisabledGroup | 199 | 207 | A7 | BACKGROUND: Laparoscopic bowel surgery was evaluated in 44 consecutive patients who underwent surgery for inflammatory bowel disease (IBD). | 128-273 | 128 | 273 | BACKGROUND: @SUBJECT$ was evaluated @PREDICAT$ 44 consecutive @OBJECT$ who underwent surgery for inflammatory bowel disease (IBD). |
Fact | preserve | 40-43 | 40-43 | T4 | for | TREATS | 40 | 43 | preserve | 26-39 | 32-39 | T2 | bowel surgery | TherapeuticOrPreventiveProcedure | 26 | 39 | preserve | 44-70 | 63-70 | T3 | inflammatory bowel disease | DiseaseOrSyndrome | 44 | 70 | A8 | Laparoscopically assisted bowel surgery for inflammatory bowel disease. | 0-71 | 0 | 71 | Laparoscopically assisted @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 218-227 | 218-227 | T16 | underwent | TREATS | 218 | 227 | preserve | 228-235 | 228-235 | T13 | surgery | TherapeuticOrPreventiveProcedure | 228 | 235 | preserve | 199-207 | 199-207 | T12 | patients | PatientOrDisabledGroup | 199 | 207 | A9 | BACKGROUND: Laparoscopic bowel surgery was evaluated in 44 consecutive patients who underwent surgery for inflammatory bowel disease (IBD). | 128-273 | 128 | 273 | BACKGROUND: Laparoscopic bowel surgery was evaluated in 44 consecutive @OBJECT$ who @PREDICAT$ @SUBJECT$ for inflammatory bowel disease (IBD). |
Fact | preserve | 1183-1186 | 1183-1186 | T68 | had | PROCESS_OF | 1,183 | 1,186 | preserve | 1201-1212 | 1201-1212 | T65 | candidiasis | DiseaseOrSyndrome | 1,201 | 1,212 | preserve | 1175-1182 | 1175-1182 | T63 | patient | PatientOrDisabledGroup | 1,175 | 1,182 | A10 | One patient in the laparoscopically assisted colectomy group had a subphrenic abscess that was drained percutaneously, and one patient had a generalized candidiasis. | 1036-1213 | 1,036 | 1,213 | One patient in the laparoscopically assisted colectomy group had a subphrenic abscess that was drained percutaneously, and one @OBJECT$ @PREDICAT$ a generalized @SUBJECT$ . |
Fact | preserve | 496-499 | 496-499 | T35 | had | PROCESS_OF | 496 | 499 | preserve | 522-525 | 522-525 | T32 | IBD | DiseaseOrSyndrome | 522 | 525 | preserve | 487-495 | 487-495 | T30 | patients | PatientOrDisabledGroup | 487 | 495 | A11 | All patients had histologically proven IBD and no prior surgery for IBD. | 483-561 | 483 | 561 | All @OBJECT$ @PREDICAT$ histologically proven @SUBJECT$ and no prior surgery for IBD. |
Fact | preserve | 842-845 | 842-845 | T59 | for | TREATS | 842 | 845 | preserve | 819-841 | 836-841 | T51 | chemotherapeutic agent | PharmacologicSubstance | 819 | 841 | preserve | 866-874 | 866-874 | T53 | patients | PatientOrDisabledGroup | 866 | 874 | A1 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used @SUBJECT$ @PREDICAT$ breast cancer @OBJECT$ . |
Fact | preserve | 728-730 | 728-730 | T56 | in | PROCESS_OF | 728 | 730 | preserve | 721-727 | 721-727 | T46 | tumors | NeoplasticProcess | 721 | 727 | preserve | 731-735 | 731-735 | T47 | mice | Mammal | 731 | 735 | A2 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing @SUBJECT$ @PREDICAT$ @OBJECT$ and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. |
Possible | preserve | 1759-1766 | 1759-1766 | T116 | inhibit | DISRUPTS | 1,759 | 1,766 | preserve | 1748-1754 | 1748-1754 | T106 | emodin | BiologicallyActiveSubstance | 1,748 | 1,754 | preserve | 1771-1777 | 1771-1777 | T107 | growth | OrganismFunction | 1,771 | 1,777 | A3 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. | 1560-1879 | 1,560 | 1,879 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as @SUBJECT$ can @PREDICAT$ the @OBJECT$ of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. |
Fact | preserve | 1713-1754 | 1740-1744 | T115 | tyrosine kinase inhibitors such as emodin | ISA | 1,713 | 1,754 | preserve | 1748-1754 | 1748-1754 | T106 | emodin | BiologicallyActiveSubstance | 1,748 | 1,754 | preserve | 1713-1739 | 1729-1739 | T105 | tyrosine kinase inhibitors | PharmacologicSubstance | 1,713 | 1,739 | A5 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. | 1560-1879 | 1,560 | 1,879 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that @OBJECT$ @PREDICAT$ @SUBJECT$ can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. |
Fact | preserve | 0-32 | 26-32 | T13 | Tyrosine kinase inhibitor emodin | ISA | 0 | 32 | preserve | 26-32 | 26-32 | T2 | emodin | BiologicallyActiveSubstance | 26 | 32 | preserve | 0-25 | 16-25 | T1 | Tyrosine kinase inhibitor | PharmacologicSubstance | 0 | 25 | A6 | Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. | 0-194 | 0 | 194 | @OBJECT$ @PREDICAT$ @SUBJECT$ suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. |
Fact | preserve | 846-874 | 866-874 | T58 | breast cancer patients | PROCESS_OF | 846 | 874 | preserve | 846-859 | 853-859 | T52 | breast cancer | NeoplasticProcess | 846 | 859 | preserve | 866-874 | 866-874 | T53 | patients | PatientOrDisabledGroup | 866 | 874 | A7 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 1960-1988 | 1982-1988 | T127 | overexpressing breast tumors | PROCESS_OF | 1,960 | 1,988 | preserve | 1975-1988 | 1982-1988 | T126 | breast tumors | NeoplasticProcess | 1,975 | 1,988 | preserve | 1960-1974 | 1960-1974 | T125 | overexpressing | GeneticFunction | 1,960 | 1,974 | A9 | The results may have important implications in chemotherapy for HER-2/neu-overexpressing breast tumors. | 1880-1989 | 1,880 | 1,989 | The results may have important implications in chemotherapy for HER-2/neu- @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 1819-1821 | 1819-1821 | T118 | in | PROCESS_OF | 1,819 | 1,821 | preserve | 1812-1818 | 1812-1818 | T111 | tumors | NeoplasticProcess | 1,812 | 1,818 | preserve | 1822-1826 | 1822-1826 | T112 | mice | Mammal | 1,822 | 1,826 | A10 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. | 1560-1879 | 1,560 | 1,879 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing @SUBJECT$ @PREDICAT$ @OBJECT$ and also sensitize these tumors to paclitaxel. |
Fact | preserve | 911-920 | 911-920 | T70 | inhibited | DISRUPTS | 911 | 920 | preserve | 890-896 | 890-896 | T61 | emodin | BiologicallyActiveSubstance | 890 | 896 | preserve | 921-933 | 927-933 | T62 | tumor growth | NeoplasticProcess | 921 | 933 | A11 | We found that emodin significantly inhibited tumor growth and prolonged survival in mice bearing HER-2/neu-overexpressing human breast cancer cells. | 876-1030 | 876 | 1,030 | We found that @SUBJECT$ significantly @PREDICAT$ @OBJECT$ and prolonged survival in mice bearing HER-2/neu-overexpressing human breast cancer cells. |
Fact | preserve | 396-431 | 422-431 | T38 | emodin, a tyrosine kinase inhibitor | DISRUPTS | 396 | 431 | preserve | 396-402 | 396-402 | T24 | emodin | BiologicallyActiveSubstance | 396 | 402 | preserve | 459-474 | 466-474 | T27 | kinase activity | MolecularFunction | 459 | 474 | A12 | We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. | 358-608 | 358 | 608 | We demonstrated previously that @SUBJECT$ @PREDICAT$ , suppresses tyrosine @OBJECT$ in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. |
Fact | preserve | 319-321 | 319-321 | T22 | in | ASSOCIATED_WITH | 319 | 321 | preserve | 223-241 | 227-241 | T17 | neu proto-oncogene | GeneOrGenome | 223 | 241 | preserve | 322-328 | 322-328 | T19 | tumors | NeoplasticProcess | 322 | 328 | A13 | Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. | 195-357 | 195 | 357 | Overexpression of the HER-2/ @SUBJECT$ , which encodes the tyrosine kinase receptor p185neu, has been observed @PREDICAT$ @OBJECT$ from breast cancer patients. |
Fact | preserve | 706-727 | 721-727 | T55 | overexpressing tumors | PROCESS_OF | 706 | 727 | preserve | 721-727 | 721-727 | T46 | tumors | NeoplasticProcess | 721 | 727 | preserve | 706-720 | 706-720 | T45 | overexpressing | GeneticFunction | 706 | 720 | A14 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu- @OBJECT$ @PREDICAT$ @SUBJECT$ in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. |
Fact | preserve | 105-107 | 105-107 | T15 | in | PROCESS_OF | 105 | 107 | preserve | 44-50 | 44-50 | T3 | growth | OrganismFunction | 44 | 50 | preserve | 108-120 | 116-120 | T8 | athymic mice | Mammal | 108 | 120 | A15 | Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. | 0-194 | 0 | 194 | Tyrosine kinase inhibitor emodin suppresses @SUBJECT$ of HER-2/neu-overexpressing breast cancer cells @PREDICAT$ @OBJECT$ and sensitizes these cells to the inhibitory effect of paclitaxel. |
Fact | preserve | 433-443 | 433-443 | T36 | suppresses | DISRUPTS | 433 | 443 | preserve | 406-431 | 422-431 | T25 | tyrosine kinase inhibitor | PharmacologicSubstance | 406 | 431 | preserve | 459-474 | 466-474 | T27 | kinase activity | MolecularFunction | 459 | 474 | A17 | We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. | 358-608 | 358 | 608 | We demonstrated previously that emodin, a @SUBJECT$ , @PREDICAT$ tyrosine @OBJECT$ in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. |
Fact | preserve | 396-431 | 422-431 | T35 | emodin, a tyrosine kinase inhibitor | ISA | 396 | 431 | preserve | 396-402 | 396-402 | T24 | emodin | BiologicallyActiveSubstance | 396 | 402 | preserve | 406-431 | 422-431 | T25 | tyrosine kinase inhibitor | PharmacologicSubstance | 406 | 431 | A19 | We demonstrated previously that emodin, a tyrosine kinase inhibitor, suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. | 358-608 | 358 | 608 | We demonstrated previously that @SUBJECT$ @PREDICAT$ @OBJECT$ , suppresses tyrosine kinase activity in HER-2/neu-overexpressing breast cancer cells and preferentially represses transformation phenotypes of these cells in vitro. |
Uncommitted | preserve | 668-675 | 668-675 | T54 | inhibit | DISRUPTS | 668 | 675 | preserve | 657-663 | 657-663 | T41 | emodin | BiologicallyActiveSubstance | 657 | 663 | preserve | 680-686 | 680-686 | T42 | growth | OrganismFunction | 680 | 686 | A21 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether @SUBJECT$ can @PREDICAT$ the @OBJECT$ of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. |
Fact | preserve | 1940-1943 | 1940-1943 | T128 | for | TREATS | 1,940 | 1,943 | preserve | 1927-1939 | 1927-1939 | T122 | chemotherapy | TherapeuticOrPreventiveProcedure | 1,927 | 1,939 | preserve | 1975-1988 | 1982-1988 | T126 | breast tumors | NeoplasticProcess | 1,975 | 1,988 | A22 | The results may have important implications in chemotherapy for HER-2/neu-overexpressing breast tumors. | 1880-1989 | 1,880 | 1,989 | The results may have important implications in @SUBJECT$ @PREDICAT$ HER-2/neu-overexpressing @OBJECT$ . |
Fact | preserve | 33-43 | 33-43 | T14 | suppresses | DISRUPTS | 33 | 43 | preserve | 26-32 | 26-32 | T2 | emodin | BiologicallyActiveSubstance | 26 | 32 | preserve | 44-50 | 44-50 | T3 | growth | OrganismFunction | 44 | 50 | A23 | Tyrosine kinase inhibitor emodin suppresses growth of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. | 0-194 | 0 | 194 | Tyrosine kinase inhibitor @SUBJECT$ @PREDICAT$ @OBJECT$ of HER-2/neu-overexpressing breast cancer cells in athymic mice and sensitizes these cells to the inhibitory effect of paclitaxel. |
Fact | preserve | 334-356 | 348-356 | T23 | breast cancer patients | PROCESS_OF | 334 | 356 | preserve | 334-347 | 341-347 | T20 | breast cancer | NeoplasticProcess | 334 | 347 | preserve | 348-356 | 348-356 | T21 | patients | PatientOrDisabledGroup | 348 | 356 | A24 | Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from breast cancer patients. | 195-357 | 195 | 357 | Overexpression of the HER-2/neu proto-oncogene, which encodes the tyrosine kinase receptor p185neu, has been observed in tumors from @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 1797-1818 | 1812-1818 | T117 | overexpressing tumors | PROCESS_OF | 1,797 | 1,818 | preserve | 1812-1818 | 1812-1818 | T111 | tumors | NeoplasticProcess | 1,812 | 1,818 | preserve | 1797-1811 | 1797-1811 | T110 | overexpressing | GeneticFunction | 1,797 | 1,811 | A25 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and also sensitize these tumors to paclitaxel. | 1560-1879 | 1,560 | 1,879 | Taken together, our results suggest that the tyrosine kinase activity of HER-2/neu is required for tumor growth and chemoresistance and that tyrosine kinase inhibitors such as emodin can inhibit the growth of HER-2/neu- @OBJECT$ @PREDICAT$ @SUBJECT$ in mice and also sensitize these tumors to paclitaxel. |
Fact | preserve | 842-845 | 842-845 | T59 | for | TREATS | 842 | 845 | preserve | 819-841 | 836-841 | T51 | chemotherapeutic agent | PharmacologicSubstance | 819 | 841 | preserve | 846-859 | 853-859 | T52 | breast cancer | NeoplasticProcess | 846 | 859 | A27 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used chemotherapeutic agent for breast cancer patients. | 609-875 | 609 | 875 | In the present study, we examined whether emodin can inhibit the growth of HER-2/neu-overexpressing tumors in mice and whether emodin can sensitize these tumors to paclitaxel, a commonly used @SUBJECT$ @PREDICAT$ @OBJECT$ patients. |
Fact | preserve | 1343-1360 | 1355-1360 | T91 | human tumor cells | PART_OF | 1,343 | 1,360 | preserve | 1349-1360 | 1355-1360 | T86 | tumor cells | Cell | 1,349 | 1,360 | preserve | 1343-1348 | 1343-1348 | T85 | human | Human | 1,343 | 1,348 | A28 | xenografts of human tumor cells expressing high levels of p185neu. | 1329-1401 | 1,329 | 1,401 | xenografts of @OBJECT$ @PREDICAT$ @SUBJECT$ expressing high levels of p185neu. |
Fact | preserve | 669-673 | 669-673 | T44 | with | PROCESS_OF | 669 | 673 | preserve | 674-701 | 691-701 | T35 | acute myocardial infarction | DiseaseOrSyndrome | 674 | 701 | preserve | 660-668 | 660-668 | T34 | patients | PatientOrDisabledGroup | 660 | 668 | A1 | On the basis of this evidence, guidelines suggest that (1) all patients with acute myocardial infarction who do not have clear contraindications should be treated within 24 hours from the onset of symptoms with intravenous beta-blockers. | 591-846 | 591 | 846 | On the basis of this evidence, guidelines suggest that (1) all @OBJECT$ @PREDICAT$ @SUBJECT$ who do not have clear contraindications should be treated within 24 hours from the onset of symptoms with intravenous beta-blockers. |
Fact | preserve | 951-974 | 965-974 | T60 | ACE inhibitor treatment | USES | 951 | 974 | preserve | 965-974 | 965-974 | T49 | treatment | TherapeuticOrPreventiveProcedure | 965 | 974 | preserve | 951-964 | 955-964 | T48 | ACE inhibitor | PharmacologicSubstance | 951 | 964 | A2 | If tolerated, the treatment should be continued for at least 2 to 3 years and perhaps longer; (2) ACE inhibitor treatment should be started during the first day after myocardial infarction in most patients after timely and careful observation of the patient's hemodynamic and clinical status and after administration of routinely recommended treatments (thrombolysis, aspirin, and beta-blockers). | 847-1274 | 847 | 1,274 | If tolerated, the treatment should be continued for at least 2 to 3 years and perhaps longer; (2) @OBJECT$ @PREDICAT$ @SUBJECT$ should be started during the first day after myocardial infarction in most patients after timely and careful observation of the patient's hemodynamic and clinical status and after administration of routinely recommended treatments (thrombolysis, aspirin, and beta-blockers). |
Fact | preserve | 1387-1416 | 1407-1416 | T77 | ACE inhibitor treatment | USES | 1,387 | 1,416 | preserve | 1407-1416 | 1407-1416 | T69 | treatment | TherapeuticOrPreventiveProcedure | 1,407 | 1,416 | preserve | 1387-1406 | 1397-1406 | T68 | ACE inhibitor | PharmacologicSubstance | 1,387 | 1,406 | A4 | In the patients showing neither clinical symptoms nor instrumental signs of left ventricular dysfunction, ACE inhibitor treatment can be stopped at the time of hospital discharge and ventricular function reevaluated after an adequate period of time. | 1275-1542 | 1,275 | 1,542 | In the patients showing neither clinical symptoms nor instrumental signs of left ventricular dysfunction, @OBJECT$ @PREDICAT$ @SUBJECT$ can be stopped at the time of hospital discharge and ventricular function reevaluated after an adequate period of time. |
Fact | preserve | 423-427 | 423-427 | T30 | with | USES | 423 | 427 | preserve | 415-422 | 415-422 | T23 | therapy | TherapeuticOrPreventiveProcedure | 415 | 422 | preserve | 446-498 | 488-498 | T25 | angiotensin-converting enzyme (ACE) inhibitors | PharmacologicSubstance | 446 | 498 | A5 | Randomized clinical trials and overviews of adjunctive therapy with beta-blockers and angiotensin-converting enzyme (ACE) inhibitors showed that these treatments may further reduce mortality rates by approximately 10%. | 354-590 | 354 | 590 | Randomized clinical trials and overviews of adjunctive @SUBJECT$ @PREDICAT$ beta-blockers and @OBJECT$ showed that these treatments may further reduce mortality rates by approximately 10%. |
Fact | preserve | 423-427 | 423-427 | T30 | with | USES | 423 | 427 | preserve | 415-422 | 415-422 | T23 | therapy | TherapeuticOrPreventiveProcedure | 415 | 422 | preserve | 428-441 | 428-441 | T24 | beta-blockers | PharmacologicSubstance | 428 | 441 | A6 | Randomized clinical trials and overviews of adjunctive therapy with beta-blockers and angiotensin-converting enzyme (ACE) inhibitors showed that these treatments may further reduce mortality rates by approximately 10%. | 354-590 | 354 | 590 | Randomized clinical trials and overviews of adjunctive @SUBJECT$ @PREDICAT$ @OBJECT$ and angiotensin-converting enzyme (ACE) inhibitors showed that these treatments may further reduce mortality rates by approximately 10%. |
Fact | preserve | 62-64 | 62-64 | T6 | in | TREATS | 62 | 64 | preserve | 27-40 | 27-40 | T2 | beta-blockers | PharmacologicSubstance | 27 | 40 | preserve | 65-68 | 65-68 | T5 | AMI | DiseaseOrSyndrome | 65 | 68 | A7 | How to use ACE-inhibitors, beta-blockers, and newer therapies in AMI. | 0-69 | 0 | 69 | How to use ACE-inhibitors, @SUBJECT$ , and newer therapies @PREDICAT$ @OBJECT$ . |
Fact | preserve | 62-64 | 62-64 | T6 | in | TREATS | 62 | 64 | preserve | 52-61 | 52-61 | T4 | therapies | TherapeuticOrPreventiveProcedure | 52 | 61 | preserve | 65-68 | 65-68 | T5 | AMI | DiseaseOrSyndrome | 65 | 68 | A8 | How to use ACE-inhibitors, beta-blockers, and newer therapies in AMI. | 0-69 | 0 | 69 | How to use ACE-inhibitors, beta-blockers, and newer @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 62-64 | 62-64 | T6 | in | TREATS | 62 | 64 | preserve | 11-25 | 11-25 | T1 | ACE-inhibitors | PharmacologicSubstance | 11 | 25 | preserve | 65-68 | 65-68 | T5 | AMI | DiseaseOrSyndrome | 65 | 68 | A9 | How to use ACE-inhibitors, beta-blockers, and newer therapies in AMI. | 0-69 | 0 | 69 | How to use @SUBJECT$ , beta-blockers, and newer therapies @PREDICAT$ @OBJECT$ . |
Fact | preserve | 1049-1051 | 1049-1051 | T61 | in | PROCESS_OF | 1,049 | 1,051 | preserve | 1027-1048 | 1038-1048 | T52 | myocardial infarction | DiseaseOrSyndrome | 1,027 | 1,048 | preserve | 1057-1065 | 1057-1065 | T53 | patients | PatientOrDisabledGroup | 1,057 | 1,065 | A10 | If tolerated, the treatment should be continued for at least 2 to 3 years and perhaps longer; (2) ACE inhibitor treatment should be started during the first day after myocardial infarction in most patients after timely and careful observation of the patient's hemodynamic and clinical status and after administration of routinely recommended treatments (thrombolysis, aspirin, and beta-blockers). | 847-1274 | 847 | 1,274 | If tolerated, the treatment should be continued for at least 2 to 3 years and perhaps longer; (2) ACE inhibitor treatment should be started during the first day after @SUBJECT$ @PREDICAT$ most @OBJECT$ after timely and careful observation of the patient's hemodynamic and clinical status and after administration of routinely recommended treatments (thrombolysis, aspirin, and beta-blockers). |
Uncommitted | preserve | 263-269 | 263-269 | T20 | reduce | PREVENTS | 263 | 269 | preserve | 229-238 | 229-238 | T14 | therapies | TherapeuticOrPreventiveProcedure | 229 | 238 | preserve | 279-287 | 279-287 | T16 | symptoms | SignOrSymptom | 279 | 287 | A11 | Besides reperfusion treatment, which is the most powerful approach to the underlying pathophysiological cause of myocardial infarction, adjunctive therapies should be considered to reduce clinical symptoms, and improve left ventricular function and mortality rates. | 70-353 | 70 | 353 | Besides reperfusion treatment, which is the most powerful approach to the underlying pathophysiological cause of myocardial infarction, adjunctive @SUBJECT$ should be considered to @PREDICAT$ clinical @OBJECT$ , and improve left ventricular function and mortality rates. |
Fact | preserve | 884-891 | 884-891 | T43 | treated | TREATS | 884 | 891 | preserve | 903-912 | 903-912 | T39 | diuretics | PharmacologicSubstance | 903 | 912 | preserve | 875-883 | 875-883 | T38 | patients | PatientOrDisabledGroup | 875 | 883 | A1 | In the case control studies, the odds ratio of renal cell carcinoma occurring in patients treated with diuretics averaged 1.55 with a 95% confidence interval of 1.42 to 1.71 (p <0.00001) compared with nonusers of diuretics. | 788-1029 | 788 | 1,029 | In the case control studies, the odds ratio of renal cell carcinoma occurring in @OBJECT$ @PREDICAT$ with @SUBJECT$ averaged 1.55 with a 95% confidence interval of 1.42 to 1.71 (p <0.00001) compared with nonusers of diuretics. |
Fact | preserve | 1878-1885 | 1878-1885 | T88 | therapy | TREATS | 1,878 | 1,885 | preserve | 1853-1858 | 1853-1858 | T83 | drugs | PharmacologicSubstance | 1,853 | 1,858 | preserve | 1889-1919 | 1910-1919 | T86 | cardiovascular disorders | DiseaseOrSyndrome | 1,889 | 1,919 | A2 | Although diuretics remain the best documented drug class to reduce morbidity and mortality in systemic hypertension, our data suggest a need for continued vigilance to assess the risk-benefit ratio of all drugs used for long-term therapy of cardiovascular disorders. | 1629-1920 | 1,629 | 1,920 | Although diuretics remain the best documented drug class to reduce morbidity and mortality in systemic hypertension, our data suggest a need for continued vigilance to assess the risk-benefit ratio of all @SUBJECT$ used for long-term @PREDICAT$ of @OBJECT$ . |
Fact | preserve | 209-215 | 209-215 | T15 | reduce | PREVENTS | 209 | 215 | preserve | 199-208 | 199-208 | T12 | Diuretics | PharmacologicSubstance | 199 | 208 | preserve | 216-246 | 237-246 | T13 | cardiovascular morbidity | DiseaseOrSyndrome | 216 | 246 | A4 | Diuretics reduce cardiovascular morbidity and mortality and constitute a cornerstone in the antihypertensive arsenal. | 199-328 | 199 | 328 | @SUBJECT$ @PREDICAT$ @OBJECT$ and mortality and constitute a cornerstone in the antihypertensive arsenal. |
Possible | preserve | 176-180 | 176-180 | T11 | risk | PREDISPOSES | 176 | 180 | preserve | 128-135 | 128-135 | T7 | disease | DiseaseOrSyndrome | 128 | 135 | preserve | 185-197 | 185-197 | T10 | malignancies | NeoplasticProcess | 185 | 197 | A5 | Several studies have suggested that systemic hypertension as a disease or its therapy could increase the risk for malignancies. | 65-198 | 65 | 198 | Several studies have suggested that systemic hypertension as a @SUBJECT$ or its therapy could increase the @PREDICAT$ for @OBJECT$ . |
Fact | preserve | 862-871 | 862-871 | T42 | occurring | OCCURS_IN | 862 | 871 | preserve | 841-861 | 852-861 | T37 | renal cell carcinoma | NeoplasticProcess | 841 | 861 | preserve | 875-883 | 875-883 | T38 | patients | PatientOrDisabledGroup | 875 | 883 | A6 | In the case control studies, the odds ratio of renal cell carcinoma occurring in patients treated with diuretics averaged 1.55 with a 95% confidence interval of 1.42 to 1.71 (p <0.00001) compared with nonusers of diuretics. | 788-1029 | 788 | 1,029 | In the case control studies, the odds ratio of @SUBJECT$ @PREDICAT$ in @OBJECT$ treated with diuretics averaged 1.55 with a 95% confidence interval of 1.42 to 1.71 (p <0.00001) compared with nonusers of diuretics. |
Uncommitted | preserve | 551-553 | 551-553 | T39 | in | ASSOCIATED_WITH | 551 | 553 | preserve | 472-479 | 472-479 | T30 | eotaxin | AminoAcidPeptideOrProtein | 472 | 479 | preserve | 561-571 | 561-571 | T38 | asthmatics | DiseaseOrSyndrome | 561 | 571 | A2 | We aimed to investigate eotaxin expression during the late-phase reaction to allergen inhalation in atopic asthmatics. | 442-572 | 442 | 572 | We aimed to investigate @SUBJECT$ expression during the late-phase reaction to allergen inhalation @PREDICAT$ atopic @OBJECT$ . |
Fact | preserve | 246-272 | 263-272 | T22 | Eotaxin is a C-C chemokine | ISA | 246 | 272 | preserve | 246-253 | 246-253 | T17 | Eotaxin | AminoAcidPeptideOrProtein | 246 | 253 | preserve | 263-272 | 263-272 | T18 | chemokine | AminoAcidPeptideOrProtein | 263 | 272 | A3 | Eotaxin is a C-C chemokine with selective activity for eosinophils and basophils. | 246-333 | 246 | 333 | @SUBJECT$ @PREDICAT$ @OBJECT$ with selective activity for eosinophils and basophils. |
Fact | preserve | 1449-1451 | 1449-1451 | T88 | of | PART_OF | 1,449 | 1,451 | preserve | 1406-1435 | 1430-1435 | T80 | terminal ductal lobular units | BodyPartOrganOrOrganComponent | 1,406 | 1,435 | preserve | 1463-1469 | 1463-1469 | T82 | breast | BodyPartOrganOrOrganComponent | 1,463 | 1,469 | A1 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the terminal ductal lobular units (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. | 1267-1549 | 1,267 | 1,549 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the @SUBJECT$ (TDLU) @PREDICAT$ the normal @OBJECT$ and also in breast tumor epithelial cells as well as some stromal cells. |
Fact | preserve | 2404-2406 | 2404-2406 | T137 | in | TREATS | 2,404 | 2,406 | preserve | 2375-2388 | 2375-2388 | T132 | antiestrogens | PharmacologicSubstance | 2,375 | 2,388 | preserve | 2419-2431 | 2425-2431 | T135 | tumor growth | NeoplasticProcess | 2,419 | 2,431 | A2 | Both aromatase inhibitors and antiestrogens were effective in suppressing tumor growth in this model. | 2338-2446 | 2,338 | 2,446 | Both aromatase inhibitors and @SUBJECT$ were effective @PREDICAT$ suppressing @OBJECT$ in this model. |
Fact | preserve | 1375-1377 | 1375-1377 | T86 | in | LOCATION_OF | 1,375 | 1,377 | preserve | 1382-1398 | 1393-1398 | T79 | epithelial cells | Cell | 1,382 | 1,398 | preserve | 1326-1335 | 1326-1335 | T78 | aromatase | AminoAcidPeptideOrProtein | 1,326 | 1,335 | A3 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the terminal ductal lobular units (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. | 1267-1549 | 1,267 | 1,549 | Using immunocytochemistry and in situ hybridization, @OBJECT$ and mRNAarom was detected mainly @PREDICAT$ the @SUBJECT$ of the terminal ductal lobular units (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. |
Fact | preserve | 2310-2320 | 2310-2320 | T130 | stimulated | AUGMENTS | 2,310 | 2,320 | preserve | 2295-2303 | 2295-2303 | T127 | estrogen | Hormone | 2,295 | 2,303 | preserve | 2321-2326 | 2321-2326 | T128 | tumor | NeoplasticProcess | 2,321 | 2,326 | A4 | Thus, the cells synthesized estrogen which stimulated tumor formation. | 2261-2337 | 2,261 | 2,337 | Thus, the cells synthesized @SUBJECT$ which @PREDICAT$ @OBJECT$ formation. |
Fact | preserve | 721-724 | 721-724 | T43 | for | USES | 721 | 724 | preserve | 725-734 | 725-734 | T42 | treatment | TherapeuticOrPreventiveProcedure | 725 | 734 | preserve | 636-645 | 636-645 | T38 | Letrozole | OrganicChemical | 636 | 645 | A5 | Letrozole (CGS 20, 269) and anastrozole (ZN 1033) have been recently approved for treatment. | 636-735 | 636 | 735 | @OBJECT$ (CGS 20, 269) and anastrozole (ZN 1033) have been recently approved @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 2485-2489 | 2485-2489 | T144 | than | compared_with | 2,485 | 2,489 | preserve | 2456-2465 | 2456-2465 | T139 | letrozole | OrganicChemical | 2,456 | 2,465 | preserve | 2490-2499 | 2490-2499 | T142 | tamoxifen | OrganicChemical | 2,490 | 2,499 | A6 | However, letrozole was more effective than tamoxifen. | 2447-2500 | 2,447 | 2,500 | However, @SUBJECT$ was more effective @PREDICAT$ @OBJECT$ . |
Fact | preserve | 865-867 | 865-867 | T61 | to | compared_with | 865 | 867 | preserve | 811-820 | 811-820 | T50 | Letrozole | OrganicChemical | 811 | 820 | preserve | 874-880 | 874-880 | T52 | megace | Hormone | 874 | 880 | A7 | Letrozole has been shown to be significantly superior to megace in overall response rates and time to treatment failure, whereas anastrozole was found to improve survival in comparison to megace. | 811-1018 | 811 | 1,018 | @SUBJECT$ has been shown to be significantly superior @PREDICAT$ @OBJECT$ in overall response rates and time to treatment failure, whereas anastrozole was found to improve survival in comparison to megace. |
Fact | preserve | 2142-2144 | 2142-2144 | T122 | in | TREATS | 2,142 | 2,144 | preserve | 2128-2141 | 2128-2141 | T115 | antiestrogens | PharmacologicSubstance | 2,128 | 2,141 | preserve | 2145-2151 | 2145-2151 | T116 | tumors | NeoplasticProcess | 2,145 | 2,151 | A8 | This model also allows evaluation of the efficacy of aromatase inhibitors and antiestrogens in tumors of estrogen receptor positive, human breast carcinoma cells transfected with the human aromatase gene. | 2044-2260 | 2,044 | 2,260 | This model also allows evaluation of the efficacy of aromatase inhibitors and @SUBJECT$ @PREDICAT$ @OBJECT$ of estrogen receptor positive, human breast carcinoma cells transfected with the human aromatase gene. |
Fact | preserve | 997-1007 | 997-1007 | T63 | comparison | compared_with | 997 | 1,007 | preserve | 952-963 | 952-963 | T57 | anastrozole | OrganicChemical | 952 | 963 | preserve | 1011-1017 | 1011-1017 | T59 | megace | Hormone | 1,011 | 1,017 | A9 | Letrozole has been shown to be significantly superior to megace in overall response rates and time to treatment failure, whereas anastrozole was found to improve survival in comparison to megace. | 811-1018 | 811 | 1,018 | Letrozole has been shown to be significantly superior to megace in overall response rates and time to treatment failure, whereas @SUBJECT$ was found to improve survival in @PREDICAT$ to @OBJECT$ . |
Fact | preserve | 214-224 | 214-224 | T21 | inactivate | INHIBITS | 214 | 224 | preserve | 154-181 | 174-181 | T11 | steroidal substrate analogs | Steroid | 154 | 181 | preserve | 229-235 | 229-235 | T14 | enzyme | Enzyme | 229 | 235 | A10 | Both steroidal substrate analogs, type I inhibitors, which inactivate the enzyme and non-steroidal competitive reversible, type II inhibitors, are now available. | 149-322 | 149 | 322 | Both @SUBJECT$ , type I inhibitors, which @PREDICAT$ the @OBJECT$ and non-steroidal competitive reversible, type II inhibitors, are now available. |
Fact | preserve | 2142-2144 | 2142-2144 | T122 | in | TREATS | 2,142 | 2,144 | preserve | 2097-2123 | 2113-2123 | T114 | aromatase inhibitors | PharmacologicSubstance | 2,097 | 2,123 | preserve | 2145-2151 | 2145-2151 | T116 | tumors | NeoplasticProcess | 2,145 | 2,151 | A11 | This model also allows evaluation of the efficacy of aromatase inhibitors and antiestrogens in tumors of estrogen receptor positive, human breast carcinoma cells transfected with the human aromatase gene. | 2044-2260 | 2,044 | 2,260 | This model also allows evaluation of the efficacy of @SUBJECT$ and antiestrogens @PREDICAT$ @OBJECT$ of estrogen receptor positive, human breast carcinoma cells transfected with the human aromatase gene. |
Fact | preserve | 721-724 | 721-724 | T43 | for | USES | 721 | 724 | preserve | 725-734 | 725-734 | T42 | treatment | TherapeuticOrPreventiveProcedure | 725 | 734 | preserve | 664-675 | 664-675 | T40 | anastrozole | OrganicChemical | 664 | 675 | A12 | Letrozole (CGS 20, 269) and anastrozole (ZN 1033) have been recently approved for treatment. | 636-735 | 636 | 735 | Letrozole (CGS 20, 269) and @OBJECT$ (ZN 1033) have been recently approved @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 545-549 | 545-549 | T37 | with | PROCESS_OF | 545 | 549 | preserve | 569-576 | 569-576 | T32 | disease | DiseaseOrSyndrome | 569 | 576 | preserve | 536-544 | 536-544 | T30 | patients | PatientOrDisabledGroup | 536 | 544 | A13 | 4-hydroxyandrostenedione (4-OHA), the first selective aromatase inhibitor, has been shown to reduce serum estrogen concentrations and cause complete and partial responses in approximately 25% of patients with hormone responsive disease who have relapsed from previous endocrine treatment. | 323-635 | 323 | 635 | 4-hydroxyandrostenedione (4-OHA), the first selective aromatase inhibitor, has been shown to reduce serum estrogen concentrations and cause complete and partial responses in approximately 25% of @OBJECT$ @PREDICAT$ hormone responsive @SUBJECT$ who have relapsed from previous endocrine treatment. |
Fact | preserve | 115-118 | 115-118 | T9 | for | TREATS | 115 | 118 | preserve | 99-108 | 99-108 | T6 | treatment | TherapeuticOrPreventiveProcedure | 99 | 108 | preserve | 134-147 | 141-147 | T7 | breast cancer | NeoplasticProcess | 134 | 147 | A14 | Inhibitors of aromatase (estrogen synthetase) have been developed as treatment for postmenopausal breast cancer. | 30-148 | 30 | 148 | Inhibitors of aromatase (estrogen synthetase) have been developed as @SUBJECT$ @PREDICAT$ postmenopausal @OBJECT$ . |
Fact | preserve | 2404-2406 | 2404-2406 | T137 | in | TREATS | 2,404 | 2,406 | preserve | 2343-2363 | 2353-2363 | T131 | aromatase inhibitors | PharmacologicSubstance | 2,343 | 2,363 | preserve | 2419-2431 | 2425-2431 | T135 | tumor growth | NeoplasticProcess | 2,419 | 2,431 | A15 | Both aromatase inhibitors and antiestrogens were effective in suppressing tumor growth in this model. | 2338-2446 | 2,338 | 2,446 | Both @SUBJECT$ and antiestrogens were effective @PREDICAT$ suppressing @OBJECT$ in this model. |
Fact | preserve | 1096-1102 | 1096-1102 | T75 | within | LOCATION_OF | 1,096 | 1,102 | preserve | 1107-1113 | 1107-1113 | T67 | breast | BodyPartOrganOrOrganComponent | 1,107 | 1,113 | preserve | 1086-1095 | 1086-1095 | T66 | aromatase | AminoAcidPeptideOrProtein | 1,086 | 1,095 | A17 | The potential of aromatase within the breast as a significant source of estrogen mediating tumor proliferation and which might determine the outcome of inhibitor treatment was explored. | 1069-1266 | 1,069 | 1,266 | The potential of @OBJECT$ @PREDICAT$ the @SUBJECT$ as a significant source of estrogen mediating tumor proliferation and which might determine the outcome of inhibitor treatment was explored. |
Fact | preserve | 55-108 | 86-95 | T8 | estrogen synthetase) have been developed as treatment | ISA | 55 | 108 | preserve | 55-74 | 64-74 | T5 | estrogen synthetase | AminoAcidPeptideOrProtein | 55 | 74 | preserve | 99-108 | 99-108 | T6 | treatment | TherapeuticOrPreventiveProcedure | 99 | 108 | A18 | Inhibitors of aromatase (estrogen synthetase) have been developed as treatment for postmenopausal breast cancer. | 30-148 | 30 | 148 | Inhibitors of aromatase ( @SUBJECT$ @PREDICAT$ @OBJECT$ for postmenopausal breast cancer. |
Fact | preserve | 1399-1401 | 1399-1401 | T87 | of | PART_OF | 1,399 | 1,401 | preserve | 1382-1398 | 1393-1398 | T79 | epithelial cells | Cell | 1,382 | 1,398 | preserve | 1406-1435 | 1430-1435 | T80 | terminal ductal lobular units | BodyPartOrganOrOrganComponent | 1,406 | 1,435 | A19 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the terminal ductal lobular units (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. | 1267-1549 | 1,267 | 1,549 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the @SUBJECT$ @PREDICAT$ the @OBJECT$ (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. |
Counterfact | preserve | 2715-2722 | 2715-2722 | T158 | effects | INTERACTS_WITH | 2,715 | 2,722 | preserve | 2751-2771 | 2761-2771 | T157 | aromatase inhibitors | PharmacologicSubstance | 2,751 | 2,771 | preserve | 2736-2745 | 2736-2745 | T156 | tamoxifen | OrganicChemical | 2,736 | 2,745 | A20 | Thus, there was no additive or synergistic effects of combining tamoxifen with aromatase inhibitors. | 2666-2772 | 2,666 | 2,772 | Thus, there was no additive or synergistic @PREDICAT$ of combining @OBJECT$ with @SUBJECT$ . |
Fact | preserve | 55-108 | 86-95 | T10 | estrogen synthetase) have been developed as treatment | TREATS | 55 | 108 | preserve | 55-74 | 64-74 | T5 | estrogen synthetase | AminoAcidPeptideOrProtein | 55 | 74 | preserve | 134-147 | 141-147 | T7 | breast cancer | NeoplasticProcess | 134 | 147 | A21 | Inhibitors of aromatase (estrogen synthetase) have been developed as treatment for postmenopausal breast cancer. | 30-148 | 30 | 148 | Inhibitors of aromatase ( @SUBJECT$ @PREDICAT$ for postmenopausal @OBJECT$ . |
Fact | preserve | 2485-2489 | 2485-2489 | T145 | than | higher_than | 2,485 | 2,489 | preserve | 2456-2465 | 2456-2465 | T139 | letrozole | OrganicChemical | 2,456 | 2,465 | preserve | 2490-2499 | 2490-2499 | T142 | tamoxifen | OrganicChemical | 2,490 | 2,499 | A22 | However, letrozole was more effective than tamoxifen. | 2447-2500 | 2,447 | 2,500 | However, @SUBJECT$ was more effective @PREDICAT$ @OBJECT$ . |
Fact | preserve | 2542-2550 | 2542-2550 | T152 | combined | COEXISTS_WITH | 2,542 | 2,550 | preserve | 2556-2565 | 2556-2565 | T147 | tamoxifen | OrganicChemical | 2,556 | 2,565 | preserve | 2510-2536 | 2526-2536 | T146 | aromatase inhibitors | PharmacologicSubstance | 2,510 | 2,536 | A23 | When the aromatase inhibitors were combined with tamoxifen, tumor growth was suppressed to about the same extent as with the aromatase inhibitors alone. | 2501-2665 | 2,501 | 2,665 | When the @OBJECT$ were @PREDICAT$ with @SUBJECT$ , tumor growth was suppressed to about the same extent as with the aromatase inhibitors alone. |
Fact | preserve | 865-867 | 865-867 | T62 | to | higher_than | 865 | 867 | preserve | 811-820 | 811-820 | T50 | Letrozole | OrganicChemical | 811 | 820 | preserve | 874-880 | 874-880 | T52 | megace | Hormone | 874 | 880 | A24 | Letrozole has been shown to be significantly superior to megace in overall response rates and time to treatment failure, whereas anastrozole was found to improve survival in comparison to megace. | 811-1018 | 811 | 1,018 | @SUBJECT$ has been shown to be significantly superior @PREDICAT$ @OBJECT$ in overall response rates and time to treatment failure, whereas anastrozole was found to improve survival in comparison to megace. |
Fact | preserve | 323-402 | 393-402 | T36 | 4-hydroxyandrostenedione (4-OHA), the first selective aromatase inhibitor | ISA | 323 | 402 | preserve | 323-347 | 323-347 | T22 | 4-hydroxyandrostenedione | OrganicChemical | 323 | 347 | preserve | 383-402 | 393-402 | T24 | aromatase inhibitor | PharmacologicSubstance | 383 | 402 | A25 | 4-hydroxyandrostenedione (4-OHA), the first selective aromatase inhibitor, has been shown to reduce serum estrogen concentrations and cause complete and partial responses in approximately 25% of patients with hormone responsive disease who have relapsed from previous endocrine treatment. | 323-635 | 323 | 635 | @SUBJECT$ @PREDICAT$ @OBJECT$ , has been shown to reduce serum estrogen concentrations and cause complete and partial responses in approximately 25% of patients with hormone responsive disease who have relapsed from previous endocrine treatment. |
Fact | preserve | 1482-1511 | 1506-1511 | T89 | breast tumor epithelial cells | PART_OF | 1,482 | 1,511 | preserve | 1495-1511 | 1506-1511 | T84 | epithelial cells | Cell | 1,495 | 1,511 | preserve | 1482-1494 | 1489-1494 | T83 | breast tumor | NeoplasticProcess | 1,482 | 1,494 | A27 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the terminal ductal lobular units (TDLU) of the normal breast and also in breast tumor epithelial cells as well as some stromal cells. | 1267-1549 | 1,267 | 1,549 | Using immunocytochemistry and in situ hybridization, aromatase and mRNAarom was detected mainly in the epithelial cells of the terminal ductal lobular units (TDLU) of the normal breast and also in @OBJECT$ @PREDICAT$ @SUBJECT$ as well as some stromal cells. |
Fact | preserve | 1563-1565 | 1563-1565 | T113 | in | LOCATION_OF | 1,563 | 1,565 | preserve | 1580-1585 | 1580-1585 | T105 | cells | Cell | 1,580 | 1,585 | preserve | 1556-1562 | 1556-1562 | T103 | VCAM-1 | AminoAcidPeptideOrProtein | 1,556 | 1,562 | A1 | The rank order of potency of GC for inhibition of the expression of VCAM-1 in BEAS-2B cells was MF congruent with FP >> BUD > TAA > HC congruent with BDP. | 1482-1648 | 1,482 | 1,648 | The rank order of potency of GC for inhibition of the expression of @OBJECT$ @PREDICAT$ BEAS-2B @SUBJECT$ was MF congruent with FP >> BUD > TAA > HC congruent with BDP. |
Fact | preserve | 1469-1480 | 1478-1480 | T98 | basophil HR | LOCATION_OF | 1,469 | 1,480 | preserve | 1469-1477 | 1469-1477 | T95 | basophil | Cell | 1,469 | 1,477 | preserve | 1478-1480 | 1478-1480 | T96 | HR | CellFunction | 1,478 | 1,480 | A2 | Three-day treatment of eosinophils with GC concentration-dependently inhibited IL-5-induced eosinophil viability, with a rank of potency almost identical to that observed with basophil HR. | 1280-1481 | 1,280 | 1,481 | Three-day treatment of eosinophils with GC concentration-dependently inhibited IL-5-induced eosinophil viability, with a rank of potency almost identical to that observed with @SUBJECT$ @PREDICAT$ @OBJECT$ . |
Fact | preserve | 355-381 | 374-381 | T38 | basophil histamine release | LOCATION_OF | 355 | 381 | preserve | 355-363 | 355-363 | T23 | basophil | Cell | 355 | 363 | preserve | 364-381 | 374-381 | T24 | histamine release | CellFunction | 364 | 381 | A4 | OBJECTIVES: We compared in vitro the inhibitory activity of synthetic GC used for topical treatment in asthma and rhinitis on basophil histamine release (HR), eosinophil viability, and expression of vascular cell adhesion molecule-1 (VCAM-1) in the human bronchial epithelial cell line BEAS-2B. | 217-535 | 217 | 535 | OBJECTIVES: We compared in vitro the inhibitory activity of synthetic GC used for topical treatment in asthma and rhinitis on @SUBJECT$ @PREDICAT$ @OBJECT$ (HR), eosinophil viability, and expression of vascular cell adhesion molecule-1 (VCAM-1) in the human bronchial epithelial cell line BEAS-2B. |
Fact | preserve | 121-131 | 121-131 | T12 | inhibitors | DISRUPTS | 121 | 131 | preserve | 89-104 | 89-104 | T4 | Glucocorticoids | Hormone | 89 | 104 | preserve | 202-215 | 207-215 | T11 | cell function | CellFunction | 202 | 215 | A9 | BACKGROUND: Glucocorticoids (GC) are potent inhibitors of peripheral blood eosinophil, basophil, and airway epithelial cell function. | 77-216 | 77 | 216 | BACKGROUND: @SUBJECT$ (GC) are potent @PREDICAT$ of peripheral blood eosinophil, basophil, and airway epithelial @OBJECT$ . |
Fact | preserve | 121-131 | 121-131 | T12 | inhibitors | DISRUPTS | 121 | 131 | preserve | 89-104 | 89-104 | T4 | Glucocorticoids | Hormone | 89 | 104 | preserve | 146-168 | 158-168 | T8 | blood eosinophil | Cell | 146 | 168 | A12 | BACKGROUND: Glucocorticoids (GC) are potent inhibitors of peripheral blood eosinophil, basophil, and airway epithelial cell function. | 77-216 | 77 | 216 | BACKGROUND: @SUBJECT$ (GC) are potent @PREDICAT$ of peripheral @OBJECT$ , basophil, and airway epithelial cell function. |
Fact | preserve | 121-131 | 121-131 | T12 | inhibitors | DISRUPTS | 121 | 131 | preserve | 89-104 | 89-104 | T4 | Glucocorticoids | Hormone | 89 | 104 | preserve | 170-178 | 170-178 | T9 | basophil | Cell | 170 | 178 | A13 | BACKGROUND: Glucocorticoids (GC) are potent inhibitors of peripheral blood eosinophil, basophil, and airway epithelial cell function. | 77-216 | 77 | 216 | BACKGROUND: @SUBJECT$ (GC) are potent @PREDICAT$ of peripheral blood eosinophil, @OBJECT$ , and airway epithelial cell function. |
Fact | preserve | 219-227 | 219-227 | T27 | compared | compared_with | 219 | 227 | preserve | 244-257 | 244-257 | T21 | beta-carotene | OrganicChemical | 244 | 257 | preserve | 268-282 | 268-282 | T22 | alpha-carotene | BiologicallyActiveSubstance | 268 | 282 | A6 | To elucidate the possible role of carotenoids and vitamin A as risk factors for Alzheimer's disease (AD), we compared serum levels of beta-carotene and alpha-carotene, and vitamin A, measured by isocratic high performance liquid chromatography, of 38 AD patients and 42 controls. | 104-401 | 104 | 401 | To elucidate the possible role of carotenoids and vitamin A as risk factors for Alzheimer's disease (AD), we @PREDICAT$ serum levels of @SUBJECT$ and @OBJECT$ , and vitamin A, measured by isocratic high performance liquid chromatography, of 38 AD patients and 42 controls. |
Fact | preserve | 72-76 | 72-76 | T10 | with | PROCESS_OF | 72 | 76 | preserve | 83-102 | 95-102 | T7 | Alzheimer's disease | DiseaseOrSyndrome | 83 | 102 | preserve | 63-71 | 63-71 | T6 | patients | PatientOrDisabledGroup | 63 | 71 | A9 | Serum levels of beta-carotene, alpha-carotene and vitamin A in patients with Alzheimer's disease. | 0-103 | 0 | 103 | Serum levels of beta-carotene, alpha-carotene and vitamin A in @OBJECT$ @PREDICAT$ @SUBJECT$ . |
Fact | preserve | 1335-1344 | 1335-1344 | T89 | receiving | ADMINISTERED_TO | 1,335 | 1,344 | preserve | 1349-1353 | 1349-1353 | T82 | drug | PharmacologicSubstance | 1,349 | 1,353 | preserve | 1326-1334 | 1326-1334 | T81 | patients | PatientOrDisabledGroup | 1,326 | 1,334 | A1 | However, discontinuation of troglitazone because of elevated liver enzyme levels occurs in approximately 2% of patients receiving the drug, and frequent monitoring of liver enzymes is required (e.g. | 1203-1419 | 1,203 | 1,419 | However, discontinuation of troglitazone because of elevated liver enzyme levels occurs in approximately 2% of @OBJECT$ @PREDICAT$ the @SUBJECT$ , and frequent monitoring of liver enzymes is required (e.g. |
Fact | preserve | 2477-2487 | 2477-2487 | T142 | management | TREATS | 2,477 | 2,487 | preserve | 2451-2463 | 2451-2463 | T139 | troglitazone | OrganicChemical | 2,451 | 2,463 | preserve | 2491-2515 | 2507-2515 | T141 | type 2 diabetes mellitus | DiseaseOrSyndrome | 2,491 | 2,515 | A2 | Drug acquisition and liver function monitoring costs, as well as potential adverse effects, are important factors that may ultimately determine the precise place of troglitazone in the management of type 2 diabetes mellitus. | 2274-2516 | 2,274 | 2,516 | Drug acquisition and liver function monitoring costs, as well as potential adverse effects, are important factors that may ultimately determine the precise place of @SUBJECT$ in the @PREDICAT$ of @OBJECT$ . |
Fact | preserve | 1875-1877 | 1875-1877 | T122 | in | TREATS | 1,875 | 1,877 | preserve | 1826-1830 | 1826-1830 | T111 | drug | PharmacologicSubstance | 1,826 | 1,830 | preserve | 1898-1922 | 1914-1922 | T114 | type 2 diabetes mellitus | DiseaseOrSyndrome | 1,898 | 1,922 | A3 | The drug has been shown to improve glycaemic control in patients with type 2 diabetes mellitus when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. | 1822-2091 | 1,822 | 2,091 | The @SUBJECT$ has been shown to improve glycaemic control @PREDICAT$ patients with @OBJECT$ when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. |
Fact | preserve | 563-567 | 563-567 | T44 | with | PROCESS_OF | 563 | 567 | preserve | 574-598 | 590-598 | T34 | type 2 diabetes mellitus | DiseaseOrSyndrome | 574 | 598 | preserve | 554-562 | 554-562 | T33 | patients | PatientOrDisabledGroup | 554 | 562 | A4 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in patients with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. | 489-754 | 489 | 754 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in @OBJECT$ @PREDICAT$ @SUBJECT$ consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. |
Fact | preserve | 2681-2683 | 2681-2683 | T158 | in | TREATS | 2,681 | 2,683 | preserve | 2625-2637 | 2625-2637 | T150 | troglitazone | OrganicChemical | 2,625 | 2,637 | preserve | 2684-2692 | 2684-2692 | T153 | patients | PatientOrDisabledGroup | 2,684 | 2,692 | A5 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, troglitazone offers an effective treatment option in patients with type 2 diabetes mellitus through its action of improving insulin sensitivity. | 2517-2781 | 2,517 | 2,781 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, @SUBJECT$ offers an effective treatment option @PREDICAT$ @OBJECT$ with type 2 diabetes mellitus through its action of improving insulin sensitivity. |
Fact | preserve | 1500-1520 | 1513-1520 | T105 | troglitazone therapy | USES | 1,500 | 1,520 | preserve | 1513-1520 | 1513-1520 | T92 | therapy | TherapeuticOrPreventiveProcedure | 1,513 | 1,520 | preserve | 1500-1512 | 1500-1512 | T91 | troglitazone | OrganicChemical | 1,500 | 1,512 | A6 | Among patients who started troglitazone therapy in 1998 (after the incorporation of a boxed warning and increased monitoring requirements in the product labelling), the estimated risk of liver-related death is approximately 1 in 100,000. | 1473-1729 | 1,473 | 1,729 | Among patients who started @OBJECT$ @PREDICAT$ @SUBJECT$ in 1998 (after the incorporation of a boxed warning and increased monitoring requirements in the product labelling), the estimated risk of liver-related death is approximately 1 in 100,000. |
Fact | preserve | 699-712 | 705-712 | T45 | serum insulin | LOCATION_OF | 699 | 712 | preserve | 699-704 | 699-704 | T38 | serum | BodySubstance | 699 | 704 | preserve | 705-712 | 705-712 | T39 | insulin | AminoAcidPeptideOrProtein | 705 | 712 | A7 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in patients with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. | 489-754 | 489 | 754 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in patients with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting @SUBJECT$ @PREDICAT$ @OBJECT$ , C-peptide and triglyceride levels. |
Fact | preserve | 551-553 | 551-553 | T43 | in | TREATS | 551 | 553 | preserve | 510-522 | 510-522 | T31 | troglitazone | OrganicChemical | 510 | 522 | preserve | 554-562 | 554-562 | T33 | patients | PatientOrDisabledGroup | 554 | 562 | A10 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in patients with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. | 489-754 | 489 | 754 | Clinical trials with @SUBJECT$ (usually 200 to 600 mg/day) @PREDICAT$ @OBJECT$ with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. |
Fact | preserve | 81-148 | 101-106 | T17 | Troglitazone is the first of a new group of oral antidiabetic drugs | ISA | 81 | 148 | preserve | 81-93 | 81-93 | T6 | Troglitazone | OrganicChemical | 81 | 93 | preserve | 130-148 | 143-148 | T11 | antidiabetic drugs | PharmacologicSubstance | 130 | 148 | A12 | Troglitazone is the first of a new group of oral antidiabetic drugs, the thiazolidinediones, and is indicated for the treatment of patients with type 2 (non-insulin-dependent) diabetes mellitus. | 81-287 | 81 | 287 | @SUBJECT$ @PREDICAT$ @OBJECT$ , the thiazolidinediones, and is indicated for the treatment of patients with type 2 (non-insulin-dependent) diabetes mellitus. |
Fact | preserve | 2580-2623 | 2605-2623 | T157 | antidiabetic agents, the thiazolidinediones | ISA | 2,580 | 2,623 | preserve | 2605-2623 | 2605-2623 | T149 | thiazolidinediones | OrganicChemical | 2,605 | 2,623 | preserve | 2580-2599 | 2593-2599 | T148 | antidiabetic agents | PharmacologicSubstance | 2,580 | 2,599 | A13 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, troglitazone offers an effective treatment option in patients with type 2 diabetes mellitus through its action of improving insulin sensitivity. | 2517-2781 | 2,517 | 2,781 | Nevertheless, as the first member of a new class of oral @OBJECT$ @PREDICAT$ @SUBJECT$ , troglitazone offers an effective treatment option in patients with type 2 diabetes mellitus through its action of improving insulin sensitivity. |
Fact | preserve | 1893-1897 | 1893-1897 | T123 | with | PROCESS_OF | 1,893 | 1,897 | preserve | 1898-1922 | 1914-1922 | T114 | type 2 diabetes mellitus | DiseaseOrSyndrome | 1,898 | 1,922 | preserve | 1884-1892 | 1884-1892 | T113 | patients | PatientOrDisabledGroup | 1,884 | 1,892 | A14 | The drug has been shown to improve glycaemic control in patients with type 2 diabetes mellitus when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. | 1822-2091 | 1,822 | 2,091 | The drug has been shown to improve glycaemic control in @OBJECT$ @PREDICAT$ @SUBJECT$ when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. |
Fact | preserve | 41-51 | 41-51 | T5 | management | TREATS | 41 | 51 | preserve | 0-12 | 0-12 | T1 | Troglitazone | OrganicChemical | 0 | 12 | preserve | 55-79 | 71-79 | T4 | type 2 diabetes mellitus | DiseaseOrSyndrome | 55 | 79 | A15 | Troglitazone: a review of its use in the management of type 2 diabetes mellitus. | 0-80 | 0 | 80 | @SUBJECT$ : a review of its use in the @PREDICAT$ of @OBJECT$ . |
Fact | preserve | 130-178 | 160-178 | T18 | antidiabetic drugs, the thiazolidinediones | ISA | 130 | 178 | preserve | 160-178 | 160-178 | T12 | thiazolidinediones | OrganicChemical | 160 | 178 | preserve | 130-148 | 143-148 | T11 | antidiabetic drugs | PharmacologicSubstance | 130 | 148 | A17 | Troglitazone is the first of a new group of oral antidiabetic drugs, the thiazolidinediones, and is indicated for the treatment of patients with type 2 (non-insulin-dependent) diabetes mellitus. | 81-287 | 81 | 287 | Troglitazone is the first of a new group of oral @OBJECT$ @PREDICAT$ @SUBJECT$ , and is indicated for the treatment of patients with type 2 (non-insulin-dependent) diabetes mellitus. |
Fact | preserve | 2693-2697 | 2693-2697 | T159 | with | PROCESS_OF | 2,693 | 2,697 | preserve | 2698-2722 | 2714-2722 | T154 | type 2 diabetes mellitus | DiseaseOrSyndrome | 2,698 | 2,722 | preserve | 2684-2692 | 2684-2692 | T153 | patients | PatientOrDisabledGroup | 2,684 | 2,692 | A18 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, troglitazone offers an effective treatment option in patients with type 2 diabetes mellitus through its action of improving insulin sensitivity. | 2517-2781 | 2,517 | 2,781 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, troglitazone offers an effective treatment option in @OBJECT$ @PREDICAT$ @SUBJECT$ through its action of improving insulin sensitivity. |
Fact | preserve | 2681-2683 | 2681-2683 | T158 | in | TREATS | 2,681 | 2,683 | preserve | 2625-2637 | 2625-2637 | T150 | troglitazone | OrganicChemical | 2,625 | 2,637 | preserve | 2698-2722 | 2714-2722 | T154 | type 2 diabetes mellitus | DiseaseOrSyndrome | 2,698 | 2,722 | A19 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, troglitazone offers an effective treatment option in patients with type 2 diabetes mellitus through its action of improving insulin sensitivity. | 2517-2781 | 2,517 | 2,781 | Nevertheless, as the first member of a new class of oral antidiabetic agents, the thiazolidinediones, @SUBJECT$ offers an effective treatment option @PREDICAT$ patients with @OBJECT$ through its action of improving insulin sensitivity. |
Fact | preserve | 551-553 | 551-553 | T43 | in | TREATS | 551 | 553 | preserve | 510-522 | 510-522 | T31 | troglitazone | OrganicChemical | 510 | 522 | preserve | 574-598 | 590-598 | T34 | type 2 diabetes mellitus | DiseaseOrSyndrome | 574 | 598 | A20 | Clinical trials with troglitazone (usually 200 to 600 mg/day) in patients with type 2 diabetes mellitus consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. | 489-754 | 489 | 754 | Clinical trials with @SUBJECT$ (usually 200 to 600 mg/day) @PREDICAT$ patients with @OBJECT$ consistently showed marked improvement in glycaemic control, as well as reductions in fasting serum insulin, C-peptide and triglyceride levels. |
Fact | preserve | 1875-1877 | 1875-1877 | T122 | in | TREATS | 1,875 | 1,877 | preserve | 1826-1830 | 1826-1830 | T111 | drug | PharmacologicSubstance | 1,826 | 1,830 | preserve | 1884-1892 | 1884-1892 | T113 | patients | PatientOrDisabledGroup | 1,884 | 1,892 | A22 | The drug has been shown to improve glycaemic control in patients with type 2 diabetes mellitus when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. | 1822-2091 | 1,822 | 2,091 | The @SUBJECT$ has been shown to improve glycaemic control @PREDICAT$ @OBJECT$ with type 2 diabetes mellitus when used as monotherapy or in combination with other oral antidiabetic drugs or insulin, and its efficacy is similar to that of glibenclamide or metformin. |
Fact | preserve | 1500-1520 | 1513-1520 | T104 | troglitazone therapy | ISA | 1,500 | 1,520 | preserve | 1500-1512 | 1500-1512 | T91 | troglitazone | OrganicChemical | 1,500 | 1,512 | preserve | 1513-1520 | 1513-1520 | T92 | therapy | TherapeuticOrPreventiveProcedure | 1,513 | 1,520 | A23 | Among patients who started troglitazone therapy in 1998 (after the incorporation of a boxed warning and increased monitoring requirements in the product labelling), the estimated risk of liver-related death is approximately 1 in 100,000. | 1473-1729 | 1,473 | 1,729 | Among patients who started @SUBJECT$ @PREDICAT$ @OBJECT$ in 1998 (after the incorporation of a boxed warning and increased monitoring requirements in the product labelling), the estimated risk of liver-related death is approximately 1 in 100,000. |
Fact | preserve | 332-339 | 332-339 | T23 | markers | PREDISPOSES | 332 | 339 | preserve | 288-291 | 288-291 | T17 | AFA | TherapeuticOrPreventiveProcedure | 288 | 291 | preserve | 343-363 | 354-363 | T19 | rheumatoid arthritis | DiseaseOrSyndrome | 343 | 363 | A1 | OBJECTIVE: Antiperinuclear factor (APF), "antikeratin antibodies" ("AKA"), and antibodies to human epidermis filaggrin (AFA), are highly specific serological markers of rheumatoid arthritis (RA), which recognise epitopes on various isoforms of (pro)filaggrin. | 162-439 | 162 | 439 | OBJECTIVE: Antiperinuclear factor (APF), "antikeratin antibodies" ("AKA"), and antibodies to human epidermis filaggrin ( @SUBJECT$ ), are highly specific serological @PREDICAT$ of @OBJECT$ (RA), which recognise epitopes on various isoforms of (pro)filaggrin. |
Fact | preserve | 108-127 | 118-127 | T10 | epidermis filaggrin | PART_OF | 108 | 127 | preserve | 118-127 | 118-127 | T6 | filaggrin | AminoAcidPeptideOrProtein | 118 | 127 | preserve | 108-117 | 108-117 | T5 | epidermis | Tissue | 108 | 117 | A3 | Anti-perinuclear factor compared with the so called "antikeratin" antibodies and antibodies to human epidermis filaggrin, in the diagnosis of arthritides. | 0-161 | 0 | 161 | Anti-perinuclear factor compared with the so called "antikeratin" antibodies and antibodies to human @OBJECT$ @PREDICAT$ @SUBJECT$ , in the diagnosis of arthritides. |
Fact | preserve | 267-286 | 277-286 | T22 | epidermis filaggrin | PART_OF | 267 | 286 | preserve | 277-286 | 277-286 | T16 | filaggrin | AminoAcidPeptideOrProtein | 277 | 286 | preserve | 267-276 | 267-276 | T15 | epidermis | Tissue | 267 | 276 | A5 | OBJECTIVE: Antiperinuclear factor (APF), "antikeratin antibodies" ("AKA"), and antibodies to human epidermis filaggrin (AFA), are highly specific serological markers of rheumatoid arthritis (RA), which recognise epitopes on various isoforms of (pro)filaggrin. | 162-439 | 162 | 439 | OBJECTIVE: Antiperinuclear factor (APF), "antikeratin antibodies" ("AKA"), and antibodies to human @OBJECT$ @PREDICAT$ @SUBJECT$ (AFA), are highly specific serological markers of rheumatoid arthritis (RA), which recognise epitopes on various isoforms of (pro)filaggrin. |
Fact | preserve | 467-531 | 517-531 | T27 | antibodies are globally named antifilaggrin autoantibodies | ISA | 467 | 531 | preserve | 517-531 | 517-531 | T26 | autoantibodies | AminoAcidPeptideOrProtein | 517 | 531 | preserve | 467-477 | 467-477 | T24 | antibodies | AminoAcidPeptideOrProtein | 467 | 477 | A6 | It was proposed that these antibodies are globally named antifilaggrin autoantibodies. | 440-532 | 440 | 532 | It was proposed that these @OBJECT$ @PREDICAT$ @SUBJECT$ . |