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[ { "id": "PMID-17306711__text", "type": "abstract", "text": [ "Impaired apoptosis of pulmonary endothelial cells is associated with intimal proliferation and irreversibility of pulmonary hypertension in congenital heart disease.\nOBJECTIVES: This study sought to assess the cellular and histologic basis of irreversible pulmonary hypertension (PHT) in the clinical setting of congenital heart disease (CHD). BACKGROUND: Although many children with CHD develop pulmonary vascular disease, it is unclear why this complication is reversible after complete repair in some cases but irreversible in others. Because failure of endothelial cell apoptosis might lead to intimal proliferation and lack of reversibility of PHT, we investigated this and other key markers of vasoactivity and angiogenesis in subjects with PHT and CHD. METHODS: We assessed antiapoptotic and proapoptotic markers in vascular and perivascular cells in lung biopsy samples from 18 patients with CHD, 7 with reversible and 11 with irreversible PHT, and 6 control patients. Immunostaining for endothelial nitric oxide synthase, vascular endothelial growth factor, and CD34 (markers of vasoactivity and neoangiogenesis) was also performed. RESULTS: The antiapoptotic protein Bcl-2 was highly expressed by pulmonary endothelial cells in all cases of irreversible PHT but in no cases of reversible PHT, nor in control patients (p less than 0.001). Intimal proliferation was present in 10 of 11 irreversible PHT cases, but never observed in reversible PHT (p less than 0.001). Similarly, perivascular inflammatory T-cells expressed more antiapoptotic proteins in irreversible PHT (p less than 0.01). Irreversible PHT cases were also more likely to show compensatory upregulation of vascular endothelial growth factor and new small vessel formation at the sites of native vessel stenosis or occlusion (p less than 0.001). CONCLUSIONS: Irreversible PHT is strongly associated with impaired endothelial cell apoptosis and antiapoptotic signaling from perivascular inflammatory cells. These changes are associated with intimal proliferation and vessel narrowing, and thereby may contribute to clinical outcomes associated with pulmonary hypertension.\n" ], "offsets": [ [ 0, 2154 ] ] } ]

[ { "id": "PMID-17306711_T1", "type": "Cell", "text": [ "pulmonary endothelial cells" ], "offsets": [ [ 22, 49 ] ], "normalized": [] }, { "id": "PMID-17306711_T2", "type": "Tissue", "text": [ "intimal" ], "offsets": [ [ 69, 76 ] ], "normalized": [] }, { "id": "PMID-17306711_T3", "type": "Organ", "text": [ "pulmonary" ], "offsets": [ [ 114, 123 ] ], "normalized": [] }, { "id": "PMID-17306711_T4", "type": "Organ", "text": [ "heart" ], "offsets": [ [ 151, 156 ] ], "normalized": [] }, { "id": "PMID-17306711_T5", "type": "Cell", "text": [ "cellular" ], "offsets": [ [ 210, 218 ] ], "normalized": [] }, { "id": "PMID-17306711_T6", "type": "Organ", "text": [ "pulmonary" ], "offsets": [ [ 256, 265 ] ], "normalized": [] }, { "id": "PMID-17306711_T7", "type": "Organ", "text": [ "heart" ], "offsets": [ [ 323, 328 ] ], "normalized": [] }, { "id": "PMID-17306711_T9", "type": "Multi-tissue_structure", "text": [ "pulmonary vascular" ], "offsets": [ [ 396, 414 ] ], "normalized": [] }, { "id": "PMID-17306711_T10", "type": "Cell", "text": [ "endothelial cell" ], "offsets": [ [ 557, 573 ] ], "normalized": [] }, { "id": "PMID-17306711_T11", "type": "Tissue", "text": [ "intimal" ], "offsets": [ [ 598, 605 ] ], "normalized": [] }, { "id": "PMID-17306711_T12", "type": "Cell", "text": [ "vascular" ], "offsets": [ [ 823, 831 ] ], "normalized": [] }, { "id": "PMID-17306711_T13", "type": "Cell", "text": [ "perivascular cells" ], "offsets": [ [ 836, 854 ] ], "normalized": [] }, { "id": "PMID-17306711_T14", "type": "Multi-tissue_structure", "text": [ "lung biopsy samples" ], "offsets": [ [ 858, 877 ] ], "normalized": [] }, { "id": "PMID-17306711_T21", "type": "Cell", "text": [ "pulmonary endothelial cells" ], "offsets": [ [ 1207, 1234 ] ], "normalized": [] }, { "id": "PMID-17306711_T23", "type": "Tissue", "text": [ "Intimal" ], "offsets": [ [ 1350, 1357 ] ], "normalized": [] }, { "id": "PMID-17306711_T24", "type": "Cell", "text": [ "perivascular inflammatory T-cells" ], "offsets": [ [ 1491, 1524 ] ], "normalized": [] }, { "id": "PMID-17306711_T26", "type": "Multi-tissue_structure", "text": [ "vessel" ], "offsets": [ [ 1736, 1742 ] ], "normalized": [] }, { "id": "PMID-17306711_T27", "type": "Multi-tissue_structure", "text": [ "vessel" ], "offsets": [ [ 1776, 1782 ] ], "normalized": [] }, { "id": "PMID-17306711_T28", "type": "Cell", "text": [ "endothelial cell" ], "offsets": [ [ 1895, 1911 ] ], "normalized": [] }, { "id": "PMID-17306711_T29", "type": "Cell", "text": [ "perivascular inflammatory cells" ], "offsets": [ [ 1955, 1986 ] ], "normalized": [] }, { "id": "PMID-17306711_T30", "type": "Tissue", "text": [ "intimal" ], "offsets": [ [ 2022, 2029 ] ], "normalized": [] }, { "id": "PMID-17306711_T31", "type": "Multi-tissue_structure", "text": [ "vessel" ], "offsets": [ [ 2048, 2054 ] ], "normalized": [] }, { "id": "PMID-17306711_T32", "type": "Organ", "text": [ "pulmonary" ], "offsets": [ [ 2130, 2139 ] ], "normalized": [] }, { "id": "PMID-17306711_T8", "type": "Multi-tissue_structure", "text": [ "sites" ], "offsets": [ [ 1760, 1765 ] ], "normalized": [] } ]

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[ { "id": "PMID-15510518__text", "type": "abstract", "text": [ "[Glaucoma and ocular ischemic syndrome--case report]\nPURPOSE: Ocular ischemic syndrome (OIS) is often poorly diagnosed and treated as primary open angle glaucoma or later on, as neovascular glaucoma. We present a 54 year old male, treated topical since 23 years for glaucoma and sent to our clinic for trabeculectomy because of rapid worsening of vision on right eye with bilateral total excavation of optic disc. MATERIAL AND METHODS: Observational case report. RESULTS: Because of typical signs of IOS (iris neovascularization, mid-peripheral dot and blot hemorrhages in both eyes, narrowed arterioles in right eye, following examinations were performed: Doppler ultrasonography of carotid arteries, digital subtractional angiography of the carotid vessels and magnetic resonance angiography. The examinations showed occlusion of the right common carotid artery and with 80% stenosis of the left common carotid artery, occlusion of abdominal aorta. After phacoemulsification with implantation of intraocular lens because of rapid intumescence cataract in the right eye, and endarterectomy of left external carotid artery, the neovascularization of the iris regressed in both eyes. CONCLUSION: In case of iris neovascularization or mid-peripheral hemorrhages the Doppler sonography of carotid arteries should be performed. Quick cooperation between ophthalmologist, radiologist and vascular surgeon following endarterectomy seems to stop progressing changes of ocular ischemic syndrome.\n" ], "offsets": [ [ 0, 1488 ] ] } ]

[ { "id": "PMID-15510518_T2", "type": "Organ", "text": [ "right eye" ], "offsets": [ [ 357, 366 ] ], "normalized": [] }, { "id": "PMID-15510518_T3", "type": "Multi-tissue_structure", "text": [ "iris" ], "offsets": [ [ 505, 509 ] ], "normalized": [] }, { "id": "PMID-15510518_T5", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 578, 582 ] ], "normalized": [] }, { "id": "PMID-15510518_T6", "type": "Multi-tissue_structure", "text": [ "arterioles" ], "offsets": [ [ 593, 603 ] ], "normalized": [] }, { "id": "PMID-15510518_T7", "type": "Organ", "text": [ "right eye" ], "offsets": [ [ 607, 616 ] ], "normalized": [] }, { "id": "PMID-15510518_T8", "type": "Multi-tissue_structure", "text": [ "carotid arteries" ], "offsets": [ [ 684, 700 ] ], "normalized": [] }, { "id": "PMID-15510518_T9", "type": "Multi-tissue_structure", "text": [ "carotid vessels" ], "offsets": [ [ 743, 758 ] ], "normalized": [] }, { "id": "PMID-15510518_T10", "type": "Multi-tissue_structure", "text": [ "right common carotid artery" ], "offsets": [ [ 836, 863 ] ], "normalized": [] }, { "id": "PMID-15510518_T11", "type": "Multi-tissue_structure", "text": [ "left common carotid artery" ], "offsets": [ [ 893, 919 ] ], "normalized": [] }, { "id": "PMID-15510518_T12", "type": "Multi-tissue_structure", "text": [ "abdominal aorta" ], "offsets": [ [ 934, 949 ] ], "normalized": [] }, { "id": "PMID-15510518_T13", "type": "Organ", "text": [ "right eye" ], "offsets": [ [ 1061, 1070 ] ], "normalized": [] }, { "id": "PMID-15510518_T14", "type": "Multi-tissue_structure", "text": [ "left external carotid artery" ], "offsets": [ [ 1094, 1122 ] ], "normalized": [] }, { "id": "PMID-15510518_T16", "type": "Multi-tissue_structure", "text": [ "iris" ], "offsets": [ [ 1154, 1158 ] ], "normalized": [] }, { "id": "PMID-15510518_T17", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 1177, 1181 ] ], "normalized": [] }, { "id": "PMID-15510518_T18", "type": "Multi-tissue_structure", "text": [ "iris" ], "offsets": [ [ 1206, 1210 ] ], "normalized": [] }, { "id": "PMID-15510518_T20", "type": "Multi-tissue_structure", "text": [ "carotid arteries" ], "offsets": [ [ 1286, 1302 ] ], "normalized": [] }, { "id": "PMID-15510518_T22", "type": "Organ", "text": [ "Ocular" ], "offsets": [ [ 62, 68 ] ], "normalized": [] }, { "id": "PMID-15510518_T24", "type": "Multi-tissue_structure", "text": [ "intraocular lens" ], "offsets": [ [ 998, 1014 ] ], "normalized": [] }, { "id": "PMID-15510518_T1", "type": "Multi-tissue_structure", "text": [ "vascular" ], "offsets": [ [ 1383, 1391 ] ], "normalized": [] }, { "id": "PMID-15510518_T29", "type": "Pathological_formation", "text": [ "neovascular glaucoma" ], "offsets": [ [ 178, 198 ] ], "normalized": [] }, { "id": "PMID-15510518_T30", "type": "Pathological_formation", "text": [ "primary open angle glaucoma" ], "offsets": [ [ 134, 161 ] ], "normalized": [] }, { "id": "PMID-15510518_T31", "type": "Pathological_formation", "text": [ "Glaucoma" ], "offsets": [ [ 1, 9 ] ], "normalized": [] }, { "id": "PMID-15510518_T32", "type": "Pathological_formation", "text": [ "glaucoma" ], "offsets": [ [ 266, 274 ] ], "normalized": [] }, { "id": "PMID-15510518_T4", "type": "Organ", "text": [ "ocular" ], "offsets": [ [ 14, 20 ] ], "normalized": [] }, { "id": "PMID-15510518_T15", "type": "Organ", "text": [ "ocular" ], "offsets": [ [ 1462, 1468 ] ], "normalized": [] } ]

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[ { "id": "PMID-17583576__text", "type": "abstract", "text": [ "Modulating metastasis by a lymphangiogenic switch in prostate cancer. \nProstate cancer dissemination is difficult to detect in the clinic, and few treatment options exist for patients with advanced-stage disease. Our aim was to investigate the role of tumor lymphangiogenesis during metastasis. Further, we implemented a noninvasive molecular imaging technique to facilitate the assessment of the metastatic process. The metastatic potentials of several human prostate cancer xenograft models, LAPC-4, LAPC-9, PC3 and CWR22Rv-1 were compared. The cells were labeled with luciferase, a bioluminescence imaging reporter gene, to enable optical imaging. After tumor implantation the animals were examined weekly during several months for the appearance of metastases. Metastatic lesions were confirmed by immunohistochemistry. Additionally, the angiogenic and lymphangiogenic profiles of the tumors were characterized. To confirm the role of lymphangiogenesis in mediating metastasis, the low-metastatic LAPC-9 tumor cells were engineered to overexpress VEGF-C, and the development of metastases was evaluated. Our results show CWR22Rv-1 and PC3 tumor cell lines to be more metastatic than LAPC-4, which in turn disseminates more readily than LAPC-9. The difference in metastatic potential correlated with the endogenous production levels of lymphangiogenic growth factor VEGF-C and the presence of tumor lymphatics. In agreement, induced overexpression of VEGF-C in LAPC-9 enhanced tumor lymphangiogenesis leading to the development of metastatic lesions. Taken together, our studies, based on a molecular imaging approach for semiquantitative detection of micrometastases, point to an important role of tumor lymphatics in the metastatic process of human prostate cancer. In particular, VEGF-C seems to play a key role in prostate cancer metastasis.\n" ], "offsets": [ [ 0, 1849 ] ] } ]

[ { "id": "PMID-17583576_T1", "type": "Cancer", "text": [ "prostate cancer" ], "offsets": [ [ 53, 68 ] ], "normalized": [] }, { "id": "PMID-17583576_T2", "type": "Cancer", "text": [ "Prostate cancer" ], "offsets": [ [ 71, 86 ] ], "normalized": [] }, { "id": "PMID-17583576_T4", "type": "Cancer", "text": [ "tumor" ], "offsets": [ [ 252, 257 ] ], "normalized": [] }, { "id": "PMID-17583576_T6", "type": "Cancer", "text": [ "prostate cancer xenograft" ], "offsets": [ [ 460, 485 ] ], "normalized": [] }, { "id": "PMID-17583576_T7", "type": "Cell", "text": [ "LAPC-4" ], "offsets": [ [ 494, 500 ] ], "normalized": [] }, { "id": "PMID-17583576_T8", "type": "Cell", "text": [ "LAPC-9" ], "offsets": [ [ 502, 508 ] ], "normalized": [] }, { "id": "PMID-17583576_T9", "type": "Cell", "text": [ "PC3" ], "offsets": [ [ 510, 513 ] ], "normalized": [] }, { "id": "PMID-17583576_T10", "type": "Cell", "text": [ "CWR22Rv-1" ], "offsets": [ [ 518, 527 ] ], "normalized": [] }, { "id": "PMID-17583576_T11", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 547, 552 ] ], "normalized": [] }, { "id": "PMID-17583576_T13", "type": "Cancer", "text": [ "tumor" ], "offsets": [ [ 657, 662 ] ], "normalized": [] }, { "id": "PMID-17583576_T15", "type": "Cancer", "text": [ "Metastatic lesions" ], "offsets": [ [ 765, 783 ] ], "normalized": [] }, { "id": "PMID-17583576_T16", "type": "Cancer", "text": [ "tumors" ], "offsets": [ [ 889, 895 ] ], "normalized": [] }, { "id": "PMID-17583576_T17", "type": "Cell", "text": [ "low-metastatic LAPC-9 tumor cells" ], "offsets": [ [ 986, 1019 ] ], "normalized": [] }, { "id": "PMID-17583576_T19", "type": "Cancer", "text": [ "metastases" ], "offsets": [ [ 1082, 1092 ] ], "normalized": [] }, { "id": "PMID-17583576_T20", "type": "Cell", "text": [ "CWR22Rv-1" ], "offsets": [ [ 1125, 1134 ] ], "normalized": [] }, { "id": "PMID-17583576_T21", "type": "Cell", "text": [ "PC3 tumor cell lines" ], "offsets": [ [ 1139, 1159 ] ], "normalized": [] }, { "id": "PMID-17583576_T22", "type": "Cell", "text": [ "LAPC-4" ], "offsets": [ [ 1187, 1193 ] ], "normalized": [] }, { "id": "PMID-17583576_T23", "type": "Cell", "text": [ "LAPC-9" ], "offsets": [ [ 1240, 1246 ] ], "normalized": [] }, { "id": "PMID-17583576_T25", "type": "Multi-tissue_structure", "text": [ "tumor lymphatics" ], "offsets": [ [ 1396, 1412 ] ], "normalized": [] }, { "id": "PMID-17583576_T27", "type": "Cell", "text": [ "LAPC-9" ], "offsets": [ [ 1464, 1470 ] ], "normalized": [] }, { "id": "PMID-17583576_T28", "type": "Cancer", "text": [ "tumor" ], "offsets": [ [ 1480, 1485 ] ], "normalized": [] }, { "id": "PMID-17583576_T29", "type": "Cancer", "text": [ "metastatic lesions" ], "offsets": [ [ 1534, 1552 ] ], "normalized": [] }, { "id": "PMID-17583576_T30", "type": "Multi-tissue_structure", "text": [ "tumor lymphatics" ], "offsets": [ [ 1702, 1718 ] ], "normalized": [] }, { "id": "PMID-17583576_T32", "type": "Cancer", "text": [ "prostate cancer" ], "offsets": [ [ 1754, 1769 ] ], "normalized": [] }, { "id": "PMID-17583576_T34", "type": "Cancer", "text": [ "prostate cancer" ], "offsets": [ [ 1821, 1836 ] ], "normalized": [] }, { "id": "PMID-17583576_T3", "type": "Cancer", "text": [ "metastases" ], "offsets": [ [ 753, 763 ] ], "normalized": [] } ]

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[ { "id": "PMC-2267190-sec-04__text", "type": "sec", "text": [ "Background\nPotato late blight, a disease caused by the oomycete pathogen Phytophthora infestans, is one of the world's most devastating crop diseases. World-wide losses due to late blight exceed several billion dollars annually [1]. Most of the potato cultivars currently grown in the United States are highly susceptible to late blight and control of this disease relies almost exclusively on fungicide applications. The most effective and environmentally sound way for controlling late blight is to incorporate natural resistance into potato cultivars. The pedigrees of many potato cultivars currently used in different countries include late blight resistant germplasm derived from Solanum demissum, Solanum andigena, and other wild species. However, most of the resistance derived from these wild species is controlled by single dominant resistance genes (R genes). These R genes are only effective in preventing the development of late blight if the invading P. infestans race contains the corresponding avirulence genes. This R gene-mediated resistance is often short-lived and is rapidly overcome by new races of the late blight pathogen.\nSolanum bulbocastanum (2n = 2x = 24) is a diploid species that has adapted in the same environment as the late blight pathogen. This wild species was characterized as possessing durable resistance against P. infestans, even under high disease pressure [2,3]. Two resistance genes, RB (Rpi-blb1) and Rpi-blb2, have been cloned from S. bulbocastanum [4-6]. Both genes confer broad-spectrum resistance against a wide range of known P. infestans races. Transgenic potato lines containing a single RB gene showed a high-level resistance in the Toluca Valley, Mexico, where the potato fields are naturally intensively infested with the most diversified P. infestans populations [7]. Most interestingly, transgenic RB plants did not show total immunity to late blight, but instead showed a marked delay in both onset of symptoms and development of lesions. Such rate-limiting resistance may put less selection pressure on the P. infestans populations and protect the durability of this resistance gene. The RB gene therefore provides an excellent model to study the mechanism of broad-spectrum and rate-limiting disease resistances. An understanding of the underlying mechanism of this type of resistance is important for developing strategies to breed durable and sustainable disease resistance.\nSeveral genes have been implicated in the regulation of R gene function. Of these genes, Rar1 and Sgt1 are among the most extensively studied genes. The Rar1 (required for Mla12 resistance) gene was first identified for its essential role in the function of a subset of Mla genes that confer resistance to barley powdery mildew [8]. The RAR1 protein contains two highly similar but distinct cysteine- and histidine-rich (CHORD) Zn2+-binding domains and was proposed to play a role in stabilizing R proteins in a confirmation that is implicated in receiving pathogen signals [9]. The Sgt1 gene (suppressor of the G2 allele of skp1) is an essential gene with multiple functions in yeast. SGT1 protein was initially identified as a RAR1-interacting partner in a yeast two-hybrid screen [10]. SGT1 may play a role in R protein accumulation [11]. Rar1 and Sgt1 genes are required in various R-gene mediated resistance against viral, bacterial, oomycete or fungal pathogens [12]. However, none of the previously studied R genes showed a race-non-specific and rate-limiting resistance phenotype as the RB gene. In addition, the role the Rar1 and Sgt1 genes are not universal and these genes are not essential for resistance involving some R genes [12,13].\nBesides the two broad-spectrum resistance genes RB and Rpi-blb2, several race-specific late blight resistance genes have also been cloned [14-16]. Numerous late blight resistance genes have recently been mapped in various potato species or populations [17-25]. However, there is almost no information available about the resistance pathways mediated by any of these genes. As an initial effort to understand the RB-mediated late blight resistance pathway, we silenced the Rar1 and Sgt1 genes using an RNAi-based approach in a potato line containing the RB gene. We demonstrated that SGT1, but not RAR1, is essential for the RB-mediated broad-spectrum resistance to potato late blight.\n" ], "offsets": [ [ 0, 4370 ] ] } ]

[ { "id": "PMC-2267190-sec-04_T2", "type": "Pathological_formation", "text": [ "lesions" ], "offsets": [ [ 1987, 1994 ] ], "normalized": [] } ]

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[ { "id": "PMID-12268797__text", "type": "abstract", "text": [ "Male role in fertility decisions in Robertsport, Liberia: an experimental exercise for policy formulation.\nThere is a tendency to believe that in African societies men are the dominant decision makers in the family. In Robertsport, Liberia, there are indications that, with respect to fertility regulation, the dominance of the husband in fertility decisions exists, but it is also apparent that many of these decisions are made jointly by both husband and wife. Education is particularly influential in the joint fertility decision-making process. The 100 husbands sampled in 1982 desired a large number of children and had experience with infant and child mortality. If family planning programs should attain their goals, men should be more involved, than at present, in every aspect of the programs. Equally important is the urgency for studies related to the role of men in fertility regulation, using adequately large samples.\n" ], "offsets": [ [ 0, 937 ] ] } ]

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[ { "id": "PMID-15192017__text", "type": "abstract", "text": [ "Lactoferrin enhances Fas expression and apoptosis in the colon mucosa of azoxymethane-treated rats. \nBovine lactoferrin, a multifunctional glycoprotein, has been shown to strongly inhibit development of azoxymethane (AOM)-induced rat colon tumors. Little, however, is known about the inhibitory mechanisms. We have demonstrated recently that lactoferrin enhances the expression of a member of the tumor necrosis factor receptor family, Fas, in the colon mucosa during both early and late stages of carcinogenesis. Thus, Fas could be involved in bovine lactoferrin-mediated inhibition of tumor development. To investigate this possibility, we studied the influence of bovine lactoferrin on Fas-mediated apoptosis with regard to expression of Fas, activation of caspase-8 and caspase-3, and DNA fragmentation in the colon mucosa of AOM-treated rats. Western blot analysis demonstrated a >2.5-fold increase in Fas protein expression, as well as elevation of the active forms of both caspase-8 and caspase-3. Immunohistochemical analysis revealed Fas-positive cells and apoptotic cells preferentially within the proximal colon region, clearly at the site of bovine lactoferrin-mediated tumor inhibition. These results suggest that apoptosis caused by elevated expression of Fas is involved in chemoprevention by lactoferrin of colon carcinogenesis.\n" ], "offsets": [ [ 0, 1345 ] ] } ]

[ { "id": "PMID-15192017_T3", "type": "Multi-tissue_structure", "text": [ "colon mucosa" ], "offsets": [ [ 57, 69 ] ], "normalized": [] }, { "id": "PMID-15192017_T11", "type": "Cancer", "text": [ "colon tumors" ], "offsets": [ [ 234, 246 ] ], "normalized": [] }, { "id": "PMID-15192017_T15", "type": "Multi-tissue_structure", "text": [ "colon mucosa" ], "offsets": [ [ 448, 460 ] ], "normalized": [] }, { "id": "PMID-15192017_T19", "type": "Cancer", "text": [ "tumor" ], "offsets": [ [ 587, 592 ] ], "normalized": [] }, { "id": "PMID-15192017_T27", "type": "Multi-tissue_structure", "text": [ "colon mucosa" ], "offsets": [ [ 814, 826 ] ], "normalized": [] }, { "id": "PMID-15192017_T34", "type": "Cell", "text": [ "Fas-positive cells" ], "offsets": [ [ 1043, 1061 ] ], "normalized": [] }, { "id": "PMID-15192017_T35", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 1076, 1081 ] ], "normalized": [] }, { "id": "PMID-15192017_T36", "type": "Organ", "text": [ "colon" ], "offsets": [ [ 1117, 1122 ] ], "normalized": [] }, { "id": "PMID-15192017_T39", "type": "Cancer", "text": [ "tumor" ], "offsets": [ [ 1182, 1187 ] ], "normalized": [] }, { "id": "PMID-15192017_T42", "type": "Organ", "text": [ "colon" ], "offsets": [ [ 1323, 1328 ] ], "normalized": [] } ]

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