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PMC-3248852-sec-15
PMC-3248852-sec-15
[ { "id": "PMC-3248852-sec-15__text", "type": "sec", "text": [ "Cation binding to yolk platelet phosvitin\nIn addition to non-heme iron [23], yolk phosvitin also contains Ca2+, Mg2+, Na+ and K+ [11]. Partially relaxed 23Na Fourier transform NMR spectra revealed the existence of at least two major intracellular compartments of NMR-visible Na+ [35]. A large fraction of the Rana oocyte Na+ was NMR-invisible and could be recovered in the yolk platelets [35]. During the first meiotic division there is a net increase in NMR-visible Na+; by completion of the second meiotic division (following fertilization), about 70% of the total Na+ becomes NMR-visible. Thus, phosvitin not only serves as a site for energy storage, but also as a storage site for iron and other ions essential for embryonic development in ponds and streams that contain little dissolved salts and minerals.\n" ], "offsets": [ [ 0, 812 ] ] } ]
[ { "id": "PMC-3248852-sec-15_T1", "type": "Cell", "text": [ "yolk platelet" ], "offsets": [ [ 18, 31 ] ], "normalized": [] }, { "id": "PMC-3248852-sec-15_T2", "type": "Developing_anatomical_structure", "text": [ "yolk" ], "offsets": [ [ 77, 81 ] ], "normalized": [] }, { "id": "PMC-3248852-sec-15_T3", "type": "Cell", "text": [ "oocyte" ], "offsets": [ [ 314, 320 ] ], "normalized": [] }, { "id": "PMC-3248852-sec-15_T4", "type": "Cell", "text": [ "yolk platelets" ], "offsets": [ [ 373, 387 ] ], "normalized": [] }, { "id": "PMC-3248852-sec-15_T5", "type": "Developing_anatomical_structure", "text": [ "embryonic" ], "offsets": [ [ 719, 728 ] ], "normalized": [] }, { "id": "PMC-3248852-sec-15_T6", "type": "Cellular_component", "text": [ "intracellular compartments" ], "offsets": [ [ 233, 259 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2983913-sec-03
PMC-2983913-sec-03
[ { "id": "PMC-2983913-sec-03__text", "type": "sec", "text": [ "Crystal data\nC24H21ClN4O2S\nM r = 464.96\nTriclinic, \na = 8.6798 (18) A\nb = 11.078 (2) A\nc = 11.372 (2) A\nalpha = 78.984 (7)degrees\nbeta = 81.867 (10)degrees\ngamma = 81.718 (11)degrees\nV = 1054.8 (4) A3\nZ = 2\nCu Kalpha radiation\nmu = 2.78 mm-1\nT = 113 K\n0.28 x 0.24 x 0.20 mm\n" ], "offsets": [ [ 0, 274 ] ] } ]
[]
[]
[]
[]
PMC-2374702-caption-19
PMC-2374702-caption-19
[ { "id": "PMC-2374702-caption-19__text", "type": "caption", "text": [ "Click here for file\n" ], "offsets": [ [ 0, 20 ] ] } ]
[]
[]
[]
[]
PMC-2660356-caption-07
PMC-2660356-caption-07
[ { "id": "PMC-2660356-caption-07__text", "type": "caption", "text": [ "Additional File 2\nFull Model Code. Full model code plus instructions for running in Berkeley Madonna(TM).\n" ], "offsets": [ [ 0, 106 ] ] } ]
[]
[]
[]
[]
PMID-19922082
PMID-19922082
[ { "id": "PMID-19922082__text", "type": "abstract", "text": [ "Effectiveness of different approaches for establishing cisplatin-induced cochlear lesions in mice.\nCONCLUSIONS:\nMouse cochleae are highly resistant to systemically administered cisplatin. However, cochlear lesions can be produced effectively in mice when cisplatin is applied locally through the round window niche or tympanum.\nOBJECTIVE:\nTo explore the optimal approach for creating cisplatin-induced cochlear lesions in mice.\nMATERIALS AND METHODS:\nCisplatin was administered to adult C57BL/6J mice via four approaches: (1) transtympanic injection, (2) round window niche injection, (3) intraperitoneal injection (i.p.) at 4 mg/kg/day for 4 consecutive days, and (4) one 15 mg/kg dose i.p. The hearing was monitored using frequency-specific auditory brainstem responses (ABRs) and distortion-product otoacoustic emissions (DPOAEs). Cochlear pathology was observed in cochleograms with Harris' hematoxylin staining.\nRESULTS:\nCisplatin applied systemically did not cause any significant ABR threshold elevation across the frequencies tested (2-32 kHz), whereas local application of cisplatin through the round window niche or tympanum resulted in significant ABR threshold elevations from high to medium frequencies. The functional changes were consistent with the cochlear pathology across groups.\n" ], "offsets": [ [ 0, 1299 ] ] } ]
[ { "id": "PMID-19922082_T1", "type": "Pathological_formation", "text": [ "cochlear lesions" ], "offsets": [ [ 73, 89 ] ], "normalized": [] }, { "id": "PMID-19922082_T2", "type": "Multi-tissue_structure", "text": [ "cochleae" ], "offsets": [ [ 118, 126 ] ], "normalized": [] }, { "id": "PMID-19922082_T3", "type": "Pathological_formation", "text": [ "cochlear lesions" ], "offsets": [ [ 197, 213 ] ], "normalized": [] }, { "id": "PMID-19922082_T4", "type": "Immaterial_anatomical_entity", "text": [ "round window niche" ], "offsets": [ [ 296, 314 ] ], "normalized": [] }, { "id": "PMID-19922082_T5", "type": "Multi-tissue_structure", "text": [ "tympanum" ], "offsets": [ [ 318, 326 ] ], "normalized": [] }, { "id": "PMID-19922082_T6", "type": "Pathological_formation", "text": [ "cochlear lesions" ], "offsets": [ [ 402, 418 ] ], "normalized": [] }, { "id": "PMID-19922082_T7", "type": "Immaterial_anatomical_entity", "text": [ "round window niche" ], "offsets": [ [ 555, 573 ] ], "normalized": [] }, { "id": "PMID-19922082_T8", "type": "Multi-tissue_structure", "text": [ "brainstem" ], "offsets": [ [ 752, 761 ] ], "normalized": [] }, { "id": "PMID-19922082_T9", "type": "Multi-tissue_structure", "text": [ "Cochlear" ], "offsets": [ [ 834, 842 ] ], "normalized": [] }, { "id": "PMID-19922082_T10", "type": "Immaterial_anatomical_entity", "text": [ "round window niche" ], "offsets": [ [ 1104, 1122 ] ], "normalized": [] }, { "id": "PMID-19922082_T11", "type": "Multi-tissue_structure", "text": [ "tympanum" ], "offsets": [ [ 1126, 1134 ] ], "normalized": [] }, { "id": "PMID-19922082_T12", "type": "Multi-tissue_structure", "text": [ "cochlear" ], "offsets": [ [ 1265, 1273 ] ], "normalized": [] } ]
[]
[]
[]
PMID-18709350
PMID-18709350
[ { "id": "PMID-18709350__text", "type": "abstract", "text": [ "[TESE and mTESE. Therapeutic options in male infertility due to testicular azoospermia].\nModern techniques of testicular sperm extraction (TESE) make it possible for an infertile man to father a child. The operations are standardized to a large extent and the underlying morphological alterations of spermatogenesis also appear to be sufficiently known. Current research is focused on prognostic factors for the testicular material that determine the sperm retrieval rate and success rates after in vitro fertilization/intracytoplasmic sperm injection (IVF-ICSI).TESE and microTESE are accepted standard operations for testicular sperm retrieval for IVF/ICSI. Predictions for effective sperm recovery are addressed.\n" ], "offsets": [ [ 0, 716 ] ] } ]
[ { "id": "PMID-18709350_T1", "type": "Cell", "text": [ "testicular sperm" ], "offsets": [ [ 110, 126 ] ], "normalized": [] }, { "id": "PMID-18709350_T2", "type": "Organ", "text": [ "testicular" ], "offsets": [ [ 412, 422 ] ], "normalized": [] }, { "id": "PMID-18709350_T3", "type": "Organ", "text": [ "testicular" ], "offsets": [ [ 64, 74 ] ], "normalized": [] }, { "id": "PMID-18709350_T4", "type": "Cell", "text": [ "sperm" ], "offsets": [ [ 451, 456 ] ], "normalized": [] }, { "id": "PMID-18709350_T5", "type": "Cell", "text": [ "sperm" ], "offsets": [ [ 536, 541 ] ], "normalized": [] }, { "id": "PMID-18709350_T6", "type": "Cell", "text": [ "testicular sperm" ], "offsets": [ [ 619, 635 ] ], "normalized": [] }, { "id": "PMID-18709350_T7", "type": "Cell", "text": [ "sperm" ], "offsets": [ [ 686, 691 ] ], "normalized": [] } ]
[]
[]
[]
PMC-1550851-caption-02
PMC-1550851-caption-02
[ { "id": "PMC-1550851-caption-02__text", "type": "caption", "text": [ "Inflammation-modulating effect of antithrombin on the endothelium. Ligation of heparan sulfate proteoglycans (HSPGs) of endothelium with antithrombin (AT) induces cellular signalling events that alter the cell's biochemical and functional responses to inflammatory stimuli (e.g. bacterial lipopolysaccharide [LPS]). Changes include reduced release of inflammatory and procoagulatory mediators (e.g. interleukin [IL]-1, IL-6, tumour necrosis factor-alpha[TNF]), tissue factor (TF), adenosine diphosphate (ADP) and cellular adhesion molecules (not shown), as well as increased release of anticoagulatory prostacyclin (prostaglandin [PG]I) or CD39/ATPDase. In neuronal tissue, protective mechanisms may by mediated via the release of calcitonin gene-related peptide and nitric oxide with the potential to affect prostacyclin release [55].\n" ], "offsets": [ [ 0, 836 ] ] } ]
[ { "id": "PMC-1550851-caption-02_T1", "type": "Tissue", "text": [ "endothelium" ], "offsets": [ [ 54, 65 ] ], "normalized": [] }, { "id": "PMC-1550851-caption-02_T2", "type": "Tissue", "text": [ "endothelium" ], "offsets": [ [ 120, 131 ] ], "normalized": [] }, { "id": "PMC-1550851-caption-02_T3", "type": "Cell", "text": [ "cellular" ], "offsets": [ [ 163, 171 ] ], "normalized": [] }, { "id": "PMC-1550851-caption-02_T4", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 205, 209 ] ], "normalized": [] }, { "id": "PMC-1550851-caption-02_T6", "type": "Cell", "text": [ "cellular" ], "offsets": [ [ 513, 521 ] ], "normalized": [] }, { "id": "PMC-1550851-caption-02_T7", "type": "Tissue", "text": [ "neuronal tissue" ], "offsets": [ [ 657, 672 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3052097-caption-01
PMC-3052097-caption-01
[ { "id": "PMC-3052097-caption-01__text", "type": "caption", "text": [ "The asymmetric unit of the title compound with the atomic labelling scheme.Displacement are drawn at the 50% probability level. H atoms are represented as small spheres of arbitrary radii. Hydrogen bonds are shown as dashed lines.\n" ], "offsets": [ [ 0, 231 ] ] } ]
[]
[]
[]
[]
PMC-3135183-sec-06
PMC-3135183-sec-06
[ { "id": "PMC-3135183-sec-06__text", "type": "sec", "text": [ "4.2. Histological Findings\nMicroscopy revealed features of a diffusely growing discohesive carcinoma, exclusively growing in the alveolar interstitium, thus expanding it, while leaving the original alveolar architecture intact (Figure 2). There was local ulceration of the pleura, while, beyond this ulcer, the tumor formed a thick cake of discohesive tumor cells lining the pleural membrane (Figure 2(c)), with only focal, microscopic invasion into the fatty tissue of the parietal pleura.\nThe tumor consisted of atypical, moderately polymorphous, and irregularly shaped tumor cells with marked discohesiveness. They featured scant eosinophilic cytoplasm and irregularly contoured and hyperchromatic nuclei, often containing one or more prominent nucleoli (Figure 2(b)). There were many mitoses and apoptoses present, but necrosis was not observed. No squamous or glandular differentiation was observed, and mucin stains (PAS-D and alcian blue) were negative. Within the tumor, there were multiple small blood-filled clefts and blood lakes. Angioinvasion in medium-sized vessels, including an artery, was demonstrated (Figure 2(d)).\nOf note, the broadened alveolar septa were lined by markedly atypical epithelial cells, yet less atypical than the interstitial carcinoma (Figures 2(a) and 2(b)). The atypia of the lining cells extended beyond the tumor front, showing a sharp demarcation with normal type I pneumocytes (Figure 2(a)), a feature characteristic to nonmucinous adenocarcinoma in situ with lepidic growth pattern (former bronchioloalveolar carcinoma, BAC) [3].\n" ], "offsets": [ [ 0, 1574 ] ] } ]
[ { "id": "PMC-3135183-sec-06_T1", "type": "Pathological_formation", "text": [ "discohesive carcinoma" ], "offsets": [ [ 79, 100 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T2", "type": "Multi-tissue_structure", "text": [ "alveolar interstitium" ], "offsets": [ [ 129, 150 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T3", "type": "Multi-tissue_structure", "text": [ "alveolar" ], "offsets": [ [ 198, 206 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T4", "type": "Multi-tissue_structure", "text": [ "pleura" ], "offsets": [ [ 273, 279 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T5", "type": "Pathological_formation", "text": [ "ulcer" ], "offsets": [ [ 300, 305 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T6", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 311, 316 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T7", "type": "Cell", "text": [ "discohesive tumor cells" ], "offsets": [ [ 340, 363 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T8", "type": "Multi-tissue_structure", "text": [ "pleural membrane" ], "offsets": [ [ 375, 391 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T9", "type": "Tissue", "text": [ "fatty tissue" ], "offsets": [ [ 454, 466 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T10", "type": "Multi-tissue_structure", "text": [ "parietal pleura" ], "offsets": [ [ 474, 489 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T11", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 495, 500 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T12", "type": "Cell", "text": [ "tumor cells" ], "offsets": [ [ 572, 583 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T13", "type": "Organism_substance", "text": [ "eosinophilic cytoplasm" ], "offsets": [ [ 633, 655 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T14", "type": "Cellular_component", "text": [ "nuclei" ], "offsets": [ [ 701, 707 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T15", "type": "Cellular_component", "text": [ "nucleoli" ], "offsets": [ [ 748, 756 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T16", "type": "Cell", "text": [ "squamous" ], "offsets": [ [ 853, 861 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T17", "type": "Cell", "text": [ "glandular" ], "offsets": [ [ 865, 874 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T18", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 972, 977 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T19", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 1005, 1010 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T20", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 1029, 1034 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T21", "type": "Multi-tissue_structure", "text": [ "vessels" ], "offsets": [ [ 1072, 1079 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T22", "type": "Multi-tissue_structure", "text": [ "artery" ], "offsets": [ [ 1094, 1100 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T23", "type": "Multi-tissue_structure", "text": [ "alveolar septa" ], "offsets": [ [ 1157, 1171 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T24", "type": "Cell", "text": [ "epithelial cells" ], "offsets": [ [ 1204, 1220 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T25", "type": "Pathological_formation", "text": [ "interstitial carcinoma" ], "offsets": [ [ 1249, 1271 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T26", "type": "Cell", "text": [ "lining cells" ], "offsets": [ [ 1315, 1327 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T27", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 1348, 1353 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T28", "type": "Cell", "text": [ "type I pneumocytes" ], "offsets": [ [ 1401, 1419 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T29", "type": "Pathological_formation", "text": [ "nonmucinous adenocarcinoma" ], "offsets": [ [ 1463, 1489 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T30", "type": "Pathological_formation", "text": [ "bronchioloalveolar carcinoma" ], "offsets": [ [ 1534, 1562 ] ], "normalized": [] }, { "id": "PMC-3135183-sec-06_T31", "type": "Pathological_formation", "text": [ "BAC" ], "offsets": [ [ 1564, 1567 ] ], "normalized": [] } ]
[]
[ { "id": "PMC-3135183-sec-06_1", "entity_ids": [ "PMC-3135183-sec-06_T30", "PMC-3135183-sec-06_T31" ] } ]
[]
PMC-2638008-sec-12
PMC-2638008-sec-12
[ { "id": "PMC-2638008-sec-12__text", "type": "sec", "text": [ "Whole-Body gamma-Irradiation\nTo evaluate differential sensitivity to irradiation, mice were exposed to gamma-irradiation (4-10 Gy, single dose) and closely monitored throughout the experimentation period. Animals were killed at the first appearance of signs of poor health. Recipients of bone marrow transplants were pre-irradiated with a total dose of 10.2 Gy (two doses of 5.1 Gy, 3 h apart). For in vivo DNA damage experiments, mice were irradiated with a single dose of 5Gy and killed after 1, 3 or 6 hours. All irradiations were carried out in a Cesium Mark1 irradiator (Shepherd Associates).\n" ], "offsets": [ [ 0, 598 ] ] } ]
[ { "id": "PMC-2638008-sec-12_T1", "type": "Multi-tissue_structure", "text": [ "bone marrow" ], "offsets": [ [ 288, 299 ] ], "normalized": [] } ]
[]
[]
[]
PMID-18995207
PMID-18995207
[ { "id": "PMID-18995207__text", "type": "abstract", "text": [ "Atypical mycobacteriosis of the larynx: an unusual clinical presentation secondary to steroids inhalation.\nVocal cords stiffness can be associated with a variety of etiologic agents, but it is rarely seen with atypical mycobacteria, for example, Mycobacterium avium complex. We report a case of a 35-year-old white woman who is and was maintained on inhaled steroids. She presented with hoarseness and low-grade fever, but her medical history was otherwise unremarkable. Laryngoscopy revealed bilateral scarring of the vocal cords. Vocal cord biopsies were performed. Histologic examination revealed unremarkable laryngeal mucosa, except for abundant subepithelial non-necrotizing granulomata. The differential diagnosis included sarcoid, Klebsiella scleroma, and tuberculosis. Special stains reviewed abundant acid-fast bacilli, later confirmed by a DNA assay on induced deep sputum, consistent with M avium complex. Subsequently, steroids were withdrawn, and the patient was treated with a multiple-drug antituberculous regimen and had a full recovery. This unusual clinical presentation of the atypical mycobacteriosis may be encountered by otolaryngologists and pathologists, and it is critical to recognize it in patients immunocompromised because of steroids.\n" ], "offsets": [ [ 0, 1266 ] ] } ]
[ { "id": "PMID-18995207_T1", "type": "Multi-tissue_structure", "text": [ "larynx" ], "offsets": [ [ 32, 38 ] ], "normalized": [] }, { "id": "PMID-18995207_T2", "type": "Multi-tissue_structure", "text": [ "vocal cords" ], "offsets": [ [ 519, 530 ] ], "normalized": [] }, { "id": "PMID-18995207_T3", "type": "Multi-tissue_structure", "text": [ "Vocal cord" ], "offsets": [ [ 532, 542 ] ], "normalized": [] }, { "id": "PMID-18995207_T4", "type": "Multi-tissue_structure", "text": [ "laryngeal mucosa" ], "offsets": [ [ 613, 629 ] ], "normalized": [] }, { "id": "PMID-18995207_T5", "type": "Pathological_formation", "text": [ "subepithelial non-necrotizing granulomata" ], "offsets": [ [ 651, 692 ] ], "normalized": [] }, { "id": "PMID-18995207_T6", "type": "Pathological_formation", "text": [ "sarcoid" ], "offsets": [ [ 730, 737 ] ], "normalized": [] }, { "id": "PMID-18995207_T7", "type": "Pathological_formation", "text": [ "Klebsiella scleroma" ], "offsets": [ [ 739, 758 ] ], "normalized": [] }, { "id": "PMID-18995207_T8", "type": "Organism_substance", "text": [ "sputum" ], "offsets": [ [ 877, 883 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3100324-sec-10
PMC-3100324-sec-10
[ { "id": "PMC-3100324-sec-10__text", "type": "sec", "text": [ "Statistics\nThe survival of mice was analyzed using Kaplan-Meier survival analysis. All other data were analyzed by one-way ANOVA, followed by the Student-Newman-Keuls test for all pairwise comparisons. Prior to ANOVA, Levene's Test for Equality of Variances was performed. All statistical analyses were performed using MedCalc software, version 11.2.1.0.\n" ], "offsets": [ [ 0, 355 ] ] } ]
[]
[]
[]
[]
PMID-11712346
PMID-11712346
[ { "id": "PMID-11712346__text", "type": "abstract", "text": [ "[Anesthetic management of a patient with Dyggve-Melchior-Clausen syndrome].\nThe Dyggve-Melchior-Clausen syndrome (DMCS) is a rare autosomal recessive skeletal dysplasia characterized by short-trunk dwarfism and mental retardation. A 49-year-old male with DMCS underwent resection arthroplasty for contracture of the right hip joint under general anesthesia using thiamylal, nitrous oxide, sevoflurane, and vecuronium. Although he was assumed to have difficult airway due to short neck, macroglossia, and disturbance of neck flexion, tracheal intubation was not difficult. No complications including malignant hyperthermia were observed during the 95 min of the operation.\n" ], "offsets": [ [ 0, 672 ] ] } ]
[ { "id": "PMID-11712346_T1", "type": "Anatomical_system", "text": [ "skeletal" ], "offsets": [ [ 150, 158 ] ], "normalized": [] }, { "id": "PMID-11712346_T2", "type": "Organism_subdivision", "text": [ "trunk" ], "offsets": [ [ 192, 197 ] ], "normalized": [] }, { "id": "PMID-11712346_T3", "type": "Multi-tissue_structure", "text": [ "airway" ], "offsets": [ [ 460, 466 ] ], "normalized": [] }, { "id": "PMID-11712346_T4", "type": "Organism_subdivision", "text": [ "neck" ], "offsets": [ [ 480, 484 ] ], "normalized": [] }, { "id": "PMID-11712346_T5", "type": "Organism_subdivision", "text": [ "neck" ], "offsets": [ [ 519, 523 ] ], "normalized": [] }, { "id": "PMID-11712346_T6", "type": "Multi-tissue_structure", "text": [ "right hip joint" ], "offsets": [ [ 316, 331 ] ], "normalized": [] }, { "id": "PMID-11712346_T7", "type": "Multi-tissue_structure", "text": [ "tracheal" ], "offsets": [ [ 533, 541 ] ], "normalized": [] } ]
[]
[]
[]
PMID-1802941
PMID-1802941
[ { "id": "PMID-1802941__text", "type": "abstract", "text": [ "M. leprae- and BCG-induced chemiluminescence response of monocytes from leprosy patients and healthy subjects: effects of gamma-interferon and GM-CSF.\nMycobacterium leprae, in contrast to BCG, failed to trigger any chemiluminescence (CL) response in mononuclear cells from either leprosy patients or healthy subjects, a deficit not reversed by either interferon-gamma or GM-CSF. Chemiluminescence responses induced without mycobacteria or with BCG were found to be lower in leprosy patients than in controls. M. leprae were also less well phagocytosed than BCG. However, there was a significant difference in phagocytosis between healthy and tuberculoid leprosy subjects. Phagocytosis was not altered by the addition of either lymphokine, and no major differences between healthy subjects and patients were observed. Preincubating mononuclear cells with anti-mycobacteria antibodies (lepromatous patients' sera) did not increase the CL response nor the phagocytosis of M. leprae or BCG.\n" ], "offsets": [ [ 0, 987 ] ] } ]
[ { "id": "PMID-1802941_T1", "type": "Cell", "text": [ "monocytes" ], "offsets": [ [ 57, 66 ] ], "normalized": [] }, { "id": "PMID-1802941_T2", "type": "Cell", "text": [ "mononuclear cells" ], "offsets": [ [ 250, 267 ] ], "normalized": [] }, { "id": "PMID-1802941_T3", "type": "Cell", "text": [ "mononuclear cells" ], "offsets": [ [ 831, 848 ] ], "normalized": [] }, { "id": "PMID-1802941_T4", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 906, 910 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3143519-caption-01
PMC-3143519-caption-01
[ { "id": "PMC-3143519-caption-01__text", "type": "caption", "text": [ "Paederus dermatitis involving the neck\n" ], "offsets": [ [ 0, 39 ] ] } ]
[ { "id": "PMC-3143519-caption-01_T1", "type": "Organism_subdivision", "text": [ "neck" ], "offsets": [ [ 34, 38 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2960999-sec-02
PMC-2960999-sec-02
[ { "id": "PMC-2960999-sec-02__text", "type": "sec", "text": [ "Experimental\n\n" ], "offsets": [ [ 0, 14 ] ] } ]
[]
[]
[]
[]
PMID-10841092
PMID-10841092
[ { "id": "PMID-10841092__text", "type": "abstract", "text": [ "Specific subgroup B adenovirus diagnosis by PCR of the fibre gene.\nOBJECTIVE:\nA highly sensitive and specific PCR assay targeting regions of the fibre gene was developed for the identification of subgroup B adenovirus strains. This is critical, since these adenovirus strains are frequently associated with severe respiratory infections in infants and new-borns.\nMETHODS:\nClinical samples from nasopharyngeal aspirates were analysed by PCR using several sets of primers corresponding to sequences of the gene coding for the fibre protein.\nRESULTS:\nThe assay allowed the detection and identification of all the genotypes of adenovirus subgroup B, based on the size of the amplified product when analysed on polyacrilamide gel electrophoresis. Specifically, one set of primers was able to amplify DNA of subgroup B but not subgroup C and E viruses.\nCONCLUSION:\nThe detection of adenovirus and the genotyping can be done on a routine basis by a PCR assay using the fibre gene as a target. The assay allows the identification of ADV subgroup B, including genotype 7h, which is the single most important viral pathogen associated with respiratory diseases in infants and young children in the southern part of South America.\n" ], "offsets": [ [ 0, 1220 ] ] } ]
[ { "id": "PMID-10841092_T1", "type": "Anatomical_system", "text": [ "respiratory" ], "offsets": [ [ 314, 325 ] ], "normalized": [] }, { "id": "PMID-10841092_T2", "type": "Organism_substance", "text": [ "nasopharyngeal aspirates" ], "offsets": [ [ 394, 418 ] ], "normalized": [] }, { "id": "PMID-10841092_T3", "type": "Anatomical_system", "text": [ "respiratory" ], "offsets": [ [ 1130, 1141 ] ], "normalized": [] }, { "id": "PMID-10841092_T4", "type": "Organism_substance", "text": [ "samples" ], "offsets": [ [ 381, 388 ] ], "normalized": [] } ]
[]
[]
[ { "id": "PMID-10841092_R1", "type": "Part-of", "arg1_id": "PMID-10841092_T4", "arg2_id": "PMID-10841092_T2", "normalized": [] } ]
PMC-3212806-sec-17
PMC-3212806-sec-17
[ { "id": "PMC-3212806-sec-17__text", "type": "sec", "text": [ "Authors' contributions\nEEKN was responsible for data collection, statistical analysis and drafting the manuscript. SAGN and YW involved in data collection and helped with the data analysis. AS helped in data analysis. EST and JL directed the study and helped in revising the manuscript. RMVD helped in data analysis, interpretation of the results and led writing of the manuscript. All authors read and approved the final manuscript.\n" ], "offsets": [ [ 0, 434 ] ] } ]
[]
[]
[]
[]
PMID-21416173
PMID-21416173
[ { "id": "PMID-21416173__text", "type": "abstract", "text": [ "Predictive value of serum carbohydrate antigen 19-9 in malignant intraductal papillary mucinous neoplasms.\nBACKGROUND:\nThe goal of the present study was to evaluate the predictive value of serum carbohydrate antigen 19-9 (CA 19-9) in the diagnosis of malignant intraductal papillary mucinous neoplasms of pancreas (IPMNs).\nMETHODS:\nEighty-six patients with pathological diagnosis of IPMNs in Zhongshan Hospital between March 1999 and November 2008 were retrospectively reviewed. Data reflecting clinical characteristics, tumor marker level, and prognosis were collected. The potential predictive value of CA 19-9 was analyzed by receiver operating characteristic (ROC) curve.\nRESULTS:\nEighty-six consecutive patients with IPMNs all underwent surgical intervention. A high level of CA 19-9 or carcinoembryonic antigen (CEA) was associated with more advanced stage of malignant IPMNs. Carbohydrate antigen 19-9 was significant for judging malignant IPMNs in the binary logistic regression model (p=0.047). The hazard ratio was 1.014, whose 95.0% confidence interval was 0.91-1.028. Receiver operating characteristic analysis showed that the serum CA 19-9 level had good predictive value for malignant or invasive IPMNs, postoperative survival, and disease-specific recurrence. The area under the curve (AUC) was 0.856, 0.893, 0.815, and 0.857 (p<0.05), respectively. According to the follow-up, mean survival time for groups with CA 19-9>63.60 U/ml was dramatically shorter than that for groups with CA 19-9<=63.60 U/ml (57.38+/-2.85 versus 29.24+/-5.82 [months]; p<0.01).\nCONCLUSIONS:\nSerum CA 19-9 level has good predictive value for malignant or invasive IPMNs. Patients with CA 19-9 > 63.60 U/ml had poor postoperative prognosis in IPMNs. Preoperative abnormal serum CA 19-9 might be predictive for an aggressive surgical intervention in IPMNs.\n" ], "offsets": [ [ 0, 1847 ] ] } ]
[ { "id": "PMID-21416173_T1", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 20, 25 ] ], "normalized": [] }, { "id": "PMID-21416173_T2", "type": "Pathological_formation", "text": [ "papillary mucinous neoplasms" ], "offsets": [ [ 77, 105 ] ], "normalized": [] }, { "id": "PMID-21416173_T3", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 189, 194 ] ], "normalized": [] }, { "id": "PMID-21416173_T4", "type": "Pathological_formation", "text": [ "intraductal papillary mucinous neoplasms" ], "offsets": [ [ 261, 301 ] ], "normalized": [] }, { "id": "PMID-21416173_T5", "type": "Organ", "text": [ "pancreas" ], "offsets": [ [ 305, 313 ] ], "normalized": [] }, { "id": "PMID-21416173_T6", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 315, 320 ] ], "normalized": [] }, { "id": "PMID-21416173_T7", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 383, 388 ] ], "normalized": [] }, { "id": "PMID-21416173_T8", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 521, 526 ] ], "normalized": [] }, { "id": "PMID-21416173_T9", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 876, 881 ] ], "normalized": [] }, { "id": "PMID-21416173_T10", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 947, 952 ] ], "normalized": [] }, { "id": "PMID-21416173_T11", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 1139, 1144 ] ], "normalized": [] }, { "id": "PMID-21416173_T12", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 1211, 1216 ] ], "normalized": [] }, { "id": "PMID-21416173_T18", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 722, 727 ] ], "normalized": [] }, { "id": "PMID-21416173_T13", "type": "Organism_substance", "text": [ "Serum" ], "offsets": [ [ 1584, 1589 ] ], "normalized": [] }, { "id": "PMID-21416173_T14", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 1656, 1661 ] ], "normalized": [] }, { "id": "PMID-21416173_T15", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 1734, 1739 ] ], "normalized": [] }, { "id": "PMID-21416173_T16", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 1763, 1768 ] ], "normalized": [] }, { "id": "PMID-21416173_T17", "type": "Pathological_formation", "text": [ "IPMNs" ], "offsets": [ [ 1840, 1845 ] ], "normalized": [] } ]
[]
[ { "id": "PMID-21416173_1", "entity_ids": [ "PMID-21416173_T4", "PMID-21416173_T6" ] } ]
[ { "id": "PMID-21416173_R1", "type": "Part-of", "arg1_id": "PMID-21416173_T4", "arg2_id": "PMID-21416173_T5", "normalized": [] } ]
PMC-2924302-sec-08
PMC-2924302-sec-08
[ { "id": "PMC-2924302-sec-08__text", "type": "sec", "text": [ "Intervention\nPatients' initial introduction to the Wrist Extension Dynasplint (WED) system, [Dynasplint Systems, Inc., Severna Park, MD, USA] included customized fitting (wrist length, width, and girth so that the force and counter force straps could be properly aligned) and training on donning and doffing of the device. (See figure 1.) Verbal and written instructions were provided throughout the duration of treatment for safety, general wear and care, and tension setting goals based on patient tolerance.\nFigure 1\nWrist Extension Dynasplint.\nEach patient initially wore the WED for 4-6 continuous hours at an initial tension setting of #2 (0.1 foot pounds of torque). This duration was for acclimatization to the system; then patients were instructed to wear the WED system at night while sleeping for 6-8 hours of continuous wear. After each patient was comfortable wearing the unit for one week at tension level #2, they were instructed to increase the tension level to #3 (0.3 ft lbs.) and make continual increases every two weeks. If prolonged soreness followed a session (soreness for more than 15 minutes) the patient was instructed to decrease the tension one half a setting for two days until they were comfortable wearing it for 6-8 hours at the new tension setting. The majority of all patients reached level #5 (0.8 foot pounds of torque) by the end of two months. All range of motion measurements were recorded by the prescribing clinician.\n" ], "offsets": [ [ 0, 1459 ] ] } ]
[ { "id": "PMC-2924302-sec-08_T1", "type": "Organism_subdivision", "text": [ "Wrist" ], "offsets": [ [ 51, 56 ] ], "normalized": [] }, { "id": "PMC-2924302-sec-08_T2", "type": "Organism_subdivision", "text": [ "wrist" ], "offsets": [ [ 171, 176 ] ], "normalized": [] }, { "id": "PMC-2924302-sec-08_T3", "type": "Organism_subdivision", "text": [ "Wrist" ], "offsets": [ [ 520, 525 ] ], "normalized": [] } ]
[]
[]
[]
PMC-1681490-sec-01
PMC-1681490-sec-01
[ { "id": "PMC-1681490-sec-01__text", "type": "sec", "text": [ "Figures and Tables\nFigure 1\nModular crosstalking in synthetic gene networks. A promoter with binding sites for lambda cI dimers (OR1 and OR2) and for the lac repressor (Olac) controls the production of the lac repressor (encoded by lacI) in module 1 and lambda cI (encoded by cI) in module 2. The lac repressor and lambda cI dimers are represented by blue ellipsoids and red circles, respectively. When the two modules are put together, two pairs of lambda cI dimers bound at different operators can loop DNA and octamerize, forming a tetramer of dimers.\n" ], "offsets": [ [ 0, 555 ] ] } ]
[]
[]
[]
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PMC-2374931-sec-01
PMC-2374931-sec-01
[ { "id": "PMC-2374931-sec-01__text", "type": "sec", "text": [ "Aim\nThis study reports the results of a large prospective single-blinded clinical trial of 3 SSRI (paroxetine, fluoxetine and escitalopram) in PE using a validated questionnaire.\n" ], "offsets": [ [ 0, 179 ] ] } ]
[]
[]
[]
[]
PMC-2811192-caption-03
PMC-2811192-caption-03
[ { "id": "PMC-2811192-caption-03__text", "type": "caption", "text": [ "Electrostatic interaction energies between the SNARE complex and fusing membranes.\n(A) Schematic diagram and definitions of intermolecular interaction energies presented in (B) and (C). In (A) through (C), only the SNARE core complex is considered. Interaction free energies are calculated for (B) a series of SNARE/membrane distances and (C) different membrane lipid compositions. Arrow in (B) indicates the most physiologically relevant distance when the closest points between SNARE and membranes are 3 A, the thickness of a layer of water.[19] In (D) through (F), TMDs of VAMP and syntaxin are present and embedded in membranes. Furthermore, the C-terminus of the SNARE motif is partially unraveled into individual alpha-helices by molecular dynamics simulations to represent trans-SNARE complex. Interaction free energies are then calculated for (E) a series of SNARE motif C-terminus separation distances and (F) different lipid compositions of the membranes. Conclusions drawn from both groups of studies are essentially the same. V (circles): Interaction energies between the SNARE complex and the v-membrane. T (squares): Interaction energies between SNARE and the t-membrane. VT (triangles): Interaction energies between the v- and the t-membranes if the SNARE complex were extracted.\n" ], "offsets": [ [ 0, 1295 ] ] } ]
[ { "id": "PMC-2811192-caption-03_T1", "type": "Cellular_component", "text": [ "membranes" ], "offsets": [ [ 72, 81 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T2", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 316, 324 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T3", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 353, 361 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T4", "type": "Cellular_component", "text": [ "membranes" ], "offsets": [ [ 490, 499 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T5", "type": "Cellular_component", "text": [ "membranes" ], "offsets": [ [ 622, 631 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T6", "type": "Cellular_component", "text": [ "membranes" ], "offsets": [ [ 955, 964 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T7", "type": "Cellular_component", "text": [ "v-membrane" ], "offsets": [ [ 1106, 1116 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T8", "type": "Cellular_component", "text": [ "t-membrane" ], "offsets": [ [ 1174, 1184 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T9", "type": "Cellular_component", "text": [ "v-" ], "offsets": [ [ 1235, 1237 ] ], "normalized": [] }, { "id": "PMC-2811192-caption-03_T10", "type": "Cellular_component", "text": [ "t-membranes" ], "offsets": [ [ 1246, 1257 ] ], "normalized": [] } ]
[]
[]
[ { "id": "PMC-2811192-caption-03_R1", "type": "frag", "arg1_id": "PMC-2811192-caption-03_T9", "arg2_id": "PMC-2811192-caption-03_T10", "normalized": [] } ]
PMC-2074286-sec-01
PMC-2074286-sec-01
[ { "id": "PMC-2074286-sec-01__text", "type": "sec", "text": [ "Images\nFigure 1\n" ], "offsets": [ [ 0, 16 ] ] } ]
[]
[]
[]
[]
PMC-3194540-sec-04
PMC-3194540-sec-04
[ { "id": "PMC-3194540-sec-04__text", "type": "sec", "text": [ "Conclusions\nThis is the first prospective evaluation of parents' preferences in newly diagnosed juvenile idiopathic arthritis patients participating in the BeSt for Kids trial. Within the limitations of the small amounts, patients clearly preferred initial combination therapy with etanercept and disliked taking prednisone. After actual exposure and follow up, this questionnaire will be repeated to see if preferences remain the same.\n" ], "offsets": [ [ 0, 437 ] ] } ]
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PMID-20525074
PMID-20525074
[ { "id": "PMID-20525074__text", "type": "abstract", "text": [ "Acoustic trauma evokes hyperactivity and changes in gene expression in guinea-pig auditory brainstem.\nHearing loss from acoustic trauma is a risk factor for tinnitus. Animal models using acoustic trauma have demonstrated hyperactivity in central auditory pathways, which has been suggested as a substrate for tinnitus. We used a guinea-pig model of unilateral acoustic trauma. Within the same animals, measurements of peripheral hearing loss, spontaneous activity of single neurons in the inferior colliculus and gene expression in cochlear nucleus and inferior colliculus were combined, acutely and after recovery from acoustic trauma. Genes investigated related to inhibitory (GABA-A receptor subunit alpha 1; glycine receptor subunit alpha 1) and excitatory neurotransmission (glutamate decarboxylase 1; glutamate receptor AMPA subunit alpha 2; glutamate receptor NMDA subunit 1), regulation of transmitter release (member of RAB family of small GTPase; RAB3 GTPase activating protein subunit 1) and neuronal excitability (potassium channel subfamily K member 15). Acoustic trauma resulted in unilateral hearing loss and hyperactivity bilaterally in inferior colliculus. Changes in expression of different mRNAs were observed in ipsilateral cochlear nucleus and in ipsi- and contralateral inferior colliculus, immediately after acoustic trauma, and after 2 and 4 weeks' recovery. Gene expression was generally reduced immediately after trauma, followed by a return to near normal levels or over-expression as recovery time increased. Different mechanisms appear to underlie the spontaneous hyperactivity observed. There is evidence of down-regulation of genes associated with neuronal inhibition in the contralateral inferior colliculus, whereas in ipsilateral cochlear nucleus, competing actions of inhibitory and excitatory systems seem to play a major role in determining overall excitability.\n" ], "offsets": [ [ 0, 1900 ] ] } ]
[ { "id": "PMID-20525074_T1", "type": "Multi-tissue_structure", "text": [ "brainstem" ], "offsets": [ [ 91, 100 ] ], "normalized": [] }, { "id": "PMID-20525074_T2", "type": "Cell", "text": [ "neurons" ], "offsets": [ [ 474, 481 ] ], "normalized": [] }, { "id": "PMID-20525074_T3", "type": "Multi-tissue_structure", "text": [ "cochlear nucleus" ], "offsets": [ [ 532, 548 ] ], "normalized": [] }, { "id": "PMID-20525074_T4", "type": "Multi-tissue_structure", "text": [ "inferior colliculus" ], "offsets": [ [ 489, 508 ] ], "normalized": [] }, { "id": "PMID-20525074_T5", "type": "Multi-tissue_structure", "text": [ "inferior colliculus" ], "offsets": [ [ 553, 572 ] ], "normalized": [] }, { "id": "PMID-20525074_T6", "type": "Cell", "text": [ "neuronal" ], "offsets": [ [ 1003, 1011 ] ], "normalized": [] }, { "id": "PMID-20525074_T7", "type": "Multi-tissue_structure", "text": [ "inferior colliculus" ], "offsets": [ [ 1153, 1172 ] ], "normalized": [] }, { "id": "PMID-20525074_T8", "type": "Multi-tissue_structure", "text": [ "cochlear nucleus" ], "offsets": [ [ 1244, 1260 ] ], "normalized": [] }, { "id": "PMID-20525074_T9", "type": "Multi-tissue_structure", "text": [ "inferior colliculus" ], "offsets": [ [ 1292, 1311 ] ], "normalized": [] }, { "id": "PMID-20525074_T10", "type": "Cell", "text": [ "neuronal" ], "offsets": [ [ 1679, 1687 ] ], "normalized": [] }, { "id": "PMID-20525074_T11", "type": "Multi-tissue_structure", "text": [ "inferior colliculus" ], "offsets": [ [ 1720, 1739 ] ], "normalized": [] }, { "id": "PMID-20525074_T12", "type": "Multi-tissue_structure", "text": [ "cochlear nucleus" ], "offsets": [ [ 1764, 1780 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2259298-sec-18
PMC-2259298-sec-18
[ { "id": "PMC-2259298-sec-18__text", "type": "sec", "text": [ "Authors' contributions\nAll authors contributed to the development of the methodology. CY and NZ led method conceptualization and prepared the original draft, which was revised by JR. CY and VD performed most implementations. All authors read and approved the final manuscript.\n" ], "offsets": [ [ 0, 277 ] ] } ]
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PMID-2512762
PMID-2512762
[ { "id": "PMID-2512762__text", "type": "abstract", "text": [ "Gastric microcirculatory change and development of acute gastric mucosal lesions (stress ulcer).\nConcerning the pathogenesis of acute gastric mucosal lesions, gastric microcirculatory change has drawn attention as an important factor. In view of this fact, gastric mucosal blood flow and microvascular structure were investigated in normal and in burn stressed rats. Moreover, alterations in acid and pepsin activities in by morphological and biochemical procedures in order to evaluate the relationship between defensive and aggressive factors of the gastric mucosa. Gastric mucosal blood flow decreased significantly in early period after induction of stress (p less than 0.01). The incidence of ulceration showed a correlative relation with the decrease of mucosal blood flow. Reduction of blood flow in burn was due to opening of arteriovenular shunt and it appeared that this was responsible for mucosal ischemia and congestion. Following the decrease of blood flow, acid output was lower in stress than that in control. Finally, the results of these studies demonstrated the importance of defensive factors. The reduction of mucosal blood flow resulted in the sequence of events that led to formation of acute gastric mucosal lesion.\n" ], "offsets": [ [ 0, 1240 ] ] } ]
[ { "id": "PMID-2512762_T1", "type": "Organ", "text": [ "Gastric" ], "offsets": [ [ 0, 7 ] ], "normalized": [] }, { "id": "PMID-2512762_T2", "type": "Pathological_formation", "text": [ "gastric mucosal lesions" ], "offsets": [ [ 57, 80 ] ], "normalized": [] }, { "id": "PMID-2512762_T3", "type": "Pathological_formation", "text": [ "stress ulcer" ], "offsets": [ [ 82, 94 ] ], "normalized": [] }, { "id": "PMID-2512762_T4", "type": "Pathological_formation", "text": [ "gastric mucosal lesions" ], "offsets": [ [ 134, 157 ] ], "normalized": [] }, { "id": "PMID-2512762_T5", "type": "Organ", "text": [ "gastric" ], "offsets": [ [ 159, 166 ] ], "normalized": [] }, { "id": "PMID-2512762_T6", "type": "Multi-tissue_structure", "text": [ "gastric mucosal" ], "offsets": [ [ 257, 272 ] ], "normalized": [] }, { "id": "PMID-2512762_T7", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 273, 278 ] ], "normalized": [] }, { "id": "PMID-2512762_T8", "type": "Tissue", "text": [ "microvascular" ], "offsets": [ [ 288, 301 ] ], "normalized": [] }, { "id": "PMID-2512762_T9", "type": "Multi-tissue_structure", "text": [ "gastric mucosa" ], "offsets": [ [ 552, 566 ] ], "normalized": [] }, { "id": "PMID-2512762_T10", "type": "Multi-tissue_structure", "text": [ "Gastric mucosal" ], "offsets": [ [ 568, 583 ] ], "normalized": [] }, { "id": "PMID-2512762_T11", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 584, 589 ] ], "normalized": [] }, { "id": "PMID-2512762_T12", "type": "Multi-tissue_structure", "text": [ "mucosal" ], "offsets": [ [ 760, 767 ] ], "normalized": [] }, { "id": "PMID-2512762_T13", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 768, 773 ] ], "normalized": [] }, { "id": "PMID-2512762_T14", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 793, 798 ] ], "normalized": [] }, { "id": "PMID-2512762_T15", "type": "Multi-tissue_structure", "text": [ "arteriovenular" ], "offsets": [ [ 834, 848 ] ], "normalized": [] }, { "id": "PMID-2512762_T16", "type": "Multi-tissue_structure", "text": [ "mucosal" ], "offsets": [ [ 901, 908 ] ], "normalized": [] }, { "id": "PMID-2512762_T17", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 960, 965 ] ], "normalized": [] }, { "id": "PMID-2512762_T18", "type": "Multi-tissue_structure", "text": [ "mucosal" ], "offsets": [ [ 1131, 1138 ] ], "normalized": [] }, { "id": "PMID-2512762_T19", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 1139, 1144 ] ], "normalized": [] }, { "id": "PMID-2512762_T20", "type": "Pathological_formation", "text": [ "gastric mucosal lesion" ], "offsets": [ [ 1216, 1238 ] ], "normalized": [] } ]
[]
[]
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PMC-2909993-sec-05
PMC-2909993-sec-05
[ { "id": "PMC-2909993-sec-05__text", "type": "sec", "text": [ "Histological analysis\nA cross-section of the distal colon (2 cm) was fixed in 10% paraformaldehyde solution. Afterwards, it was cut into small fragments, dehydrated through an ethanol series (70%-100%), cleared in xylol and embedded in paraffin. The fragments were sliced into 5 mum thick sections and stained with hematoxylin-eosin. Histological evaluation was done by a pathologist who was blinded to the experimental groups, and it was based on the intensity of mononuclear and polymorphonuclear infiltrates in the lamina propria, crypt dilation, cellular destruction and mucosal ulceration. Histopathological changes were graded according to the degree of inflammation using the following scale: absent (0), light (1), moderate (2) and intense (3), and the numbers represented the inflammation score (IS). Results were expressed as mean values of IS +/- standard error of the mean (SEM) for each experimental group.\n" ], "offsets": [ [ 0, 920 ] ] } ]
[ { "id": "PMC-2909993-sec-05_T1", "type": "Multi-tissue_structure", "text": [ "distal colon" ], "offsets": [ [ 45, 57 ] ], "normalized": [] }, { "id": "PMC-2909993-sec-05_T2", "type": "Multi-tissue_structure", "text": [ "fragments" ], "offsets": [ [ 250, 259 ] ], "normalized": [] }, { "id": "PMC-2909993-sec-05_T3", "type": "Tissue", "text": [ "lamina propria" ], "offsets": [ [ 518, 532 ] ], "normalized": [] }, { "id": "PMC-2909993-sec-05_T5", "type": "Cell", "text": [ "cellular" ], "offsets": [ [ 550, 558 ] ], "normalized": [] }, { "id": "PMC-2909993-sec-05_T6", "type": "Multi-tissue_structure", "text": [ "mucosal" ], "offsets": [ [ 575, 582 ] ], "normalized": [] }, { "id": "PMC-2909993-sec-05_T7", "type": "Immaterial_anatomical_entity", "text": [ "crypt" ], "offsets": [ [ 534, 539 ] ], "normalized": [] } ]
[]
[]
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PMC-3088328-sec-10
PMC-3088328-sec-10
[ { "id": "PMC-3088328-sec-10__text", "type": "sec", "text": [ "Etymology.\nProfessor Stephen Lane Wood worked extensively on collections of Scolytinae preserved in Indian museums, and described a number of new Scolytinae species from India. In this paper we describe one more new bark-beetle species from India kept in the Natural History Museum in Vienna (NHMW) and dedicate this species to the late Professor Stephen Lane Wood.\n" ], "offsets": [ [ 0, 366 ] ] } ]
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PMC-2193592-sec-11
PMC-2193592-sec-11
[ { "id": "PMC-2193592-sec-11__text", "type": "sec", "text": [ "Stimulation/Inhibition of iDC Functions by Activated NK Cells.\nTwo previous studies have shown that both resting and activated NK cells partially kill autologous DCs, as measured by 3-4-h chromium release assays using high NK/DC ratios (11, 12). However, in our long-term cultures (24-48 h) the NK cells stimulated the iDCs rather than lysing them. Based on these conflicting results, we examined in more detail the apparent stimulation of iDCs after contact with NK cells. We reasoned that activated NK cells would be more useful for these experiments because (i) an encounter in vivo between NK cells that normally traffic in the blood (4) and iDCs which reside in the tissues (1, 3), should only occur when both cells are activated; (ii) activated NK cells mediate more potent lysis of iDCs (11-13), thereby allowing for a more rigorous examination of a potential cytotoxic effect; and (iii) the number of NK cells obtained after short-term in vitro culture would be far greater providing more cells for analysis (9).\nThe DC maturation induced by resting NK cells we observed was dependent on endogenous TNF-alpha production. Furthermore, TNF-alpha and other proinflammatory cytokines are important amplifiers of immune responses (14). Therefore, we used TNF-alpha production as a readout for DC stimulation in our culture system. Culturing activated NK cells with DCs at low NK/DC ratios (1:5) led to increases in TNF-alpha production, which were augmented dramatically by the addition of suboptimal doses (10 ng/ml) of LPS (Fig. 2 A). The increased TNF-alpha production was dependent on cell-to-cell contact because when the two cell types were separated in trans-wells, no stimulation was observed (Fig. 2 B). In separate experiments we observed this NK-stimulatory effect on TNF-alpha production at NK/DC ratios as low as 1:20 and 1:40 (data not shown). Raising the NK/DC ratio to 5:1 changes the interaction from one of potent DC stimulation to that of complete inhibition in the presence or absence of LPS (Fig. 2 C). An identical pattern is seen for IL-12 p40 production (Fig. 2 D). No IL-10 production in the cultures was detected under any of the conditions tested (data not shown). The massive production of TNF-alpha in the cultures at the lowest ratios was mediated primarily by DCs in the culture due to the low number of NK cells (2 x 104 cells per well) used in these experiments. In addition, efforts to stimulate NK cells directly with optimal doses of anti-CD16, rIL-2, rIL-12, and PMA/ionomycin alone or in combination induced only moderate (<500 pg/ml) TNF-alpha production by the NK cells alone which were present at 2 x 105 cells per well (data not shown).\nFigure 2.\nActivated/cultured NK cell-mediated amplification/inhibition of DC cytokine production. Results are presented on log scales. Cultured iDCs were incubated alone or with cultured/purified NK cells for 24 h (A and B) or 48 h (C-E) in the presence or absence of the indicated concentrations of LPS. After culture the supernatants were removed and analyzed by ELISA for TNF-alpha or IL-12 p40. (A) TNF-alpha production was measured in the supernatants from cultures of: DCs alone (gray bars); NK+DC (1:5) (black bars). LPS concentrations used were: 0, 10, and 1,000 ng/ml (DCs alone only). (B) Contact-dependent stimulation of iDC TNF-alpha production by NK cells was tested under the following conditions: DCs alone (gray bars); NK+DC (1:5) (black bars); NK/DC (1:5) trans-wells (striped bars). LPS concentrations used were: 10 ng/ml (donor 1) and 20 ng/ml (donor 2). (C and D) Effect of increasing the NK/DC ratio (DCs alone; NK:DC-1:5; 1:1; 5:1) on (C) TNF-alpha and (D) IL-12 p40 production. LPS concentrations used were: 0 ng/ml (*); 20 ng/ml (*); 50 ng/ml (^); and 1,000 ng/ml-LPS (*) (DCs alone only). (E) The effect of neutralizing IFN-gamma production was tested under the following conditions: DCs alone (gray bars); NK+DC (1:5) (black bars); NK+DC (1:5) and 10 mug/ml of blocking anti-IFN-gamma mAb (stippled bars). LPS concentrations used were: 0 ng/ml (NO LPS) and 20 ng/ml (LPS 20).\nBlocking reagents for CD80, CD86, CD154, CD95, CD11a, CD50, or IL-12, had no effect on the NK cell-induced TNF-alpha or IL-12 p40 production, whereas a neutralizing antibody for IFN-gamma while not affecting TNF-alpha production partially blocked (<20%) IL-12 p40 production induced by the NK cells (Fig. 2 E). This partial inhibition is consistent with numerous previous reports demonstrating a central role for an IL-12/IFN-gamma positive feedback loop active between NK cells and IL-12-producing cells (15-17). Clearly, however, this well-described cytokine cross-talk mechanism is secondary to the contact-dependent activation of DCs by NK cells described here. Taken together these results indicate that novel mechanisms control cognate interactions between NK cells and DCs and that NK-DC contact has the potential to serve as an important control switch for both amplifying and attenuating innate immune responses in vivo.\nWe next tested directly whether NK cell killing was active in our system using both short-term (4-h) chromium release assays (data not shown) and a flow cytometric assay which allowed us to follow the survival of the autologous iDCs in the presence of NK cells over longer periods (Fig. 3). The results demonstrate that NK cells kill autologous iDCs (Fig. 3 A) at all NK/DC ratios tested after 4 h and the level of killing is similar to the lysis of K562 cells over the same time (Fig. 3 B). After 24 h, however, the presence of NK cells led to completely divergent effects on the DCs. At the 5:1 (NK/DC) ratio, NK cell-mediated destruction of the iDCs was the dominant feature, whereas at the low ratio (1:5) the same NK cells promoted iDCs survival compared with iDCs alone over the same period (Fig. 3 A). The equal ratio of NK/DC (1:1) fell between these two extremes. The NK cell-mediated lysis of the K562 targets increased at all ratios tested after the 24-h incubation. These striking differences between death and survival of DCs upon encountering NK cells correlate precisely with our previous results on TNF-alpha and IL-12 p40 production where increasing numbers of NK cells in the culture shifts the NK effect from potent stimulation to complete inhibition (Fig. 2).\nFigure 3.\nActivated/cultured NK cell-mediated death/survival of DCs and NK-DC conjugate formation. NK cell mediated killing/survival of CFDA.SE-loaded iDCs (A) and K562 cells (B) was measured by flow cytometry over 4 h (*) or 24 h (*) at the indicated NK/DC ratios as described in Materials and Methods. Results are presented as percentage of specific lysis +/- SEM (n = 3 independent experiments). NK-DC (C-E) or NK-K562 (F-H) conjugate formation was measured by flow cytometry, at the following ratios (NK/DC or NK/K562): 1:5 (C and F); 1:1 (D and G); and 5:1 (E and H). Snarf-1 (FL3)-labeled iDCs or K562 cells were incubated (30 min) with CFDA.SE (FL1)-labeled NK cells at the different ratios. The percentage of conjugates formed (top right quadrant) was calculated by determining the percentage of FL3+ (Snarf-1) events which were also positive for FL1 (CFDA.SE). The results are representative of four experiments performed with activated NK cells. Resting NK cells also readily formed conjugates with autologous iDCs (data not shown).\nNK cells can both efficiently kill and potently stimulate DCs in our model system and each of these opposing effects appear dependent on cell-to-cell contact. To quantify these apparent cognate interactions we measured the formation of NK-DC conjugates and compared them to conjugates formed by NK cells and tumor targets. Our analysis revealed that NK cells bound DC (Fig. 3 C-E) with an efficiency almost equal to that of NK cell binding to the classical NK-target, K562 (Fig. 3 F-H). Binding was detectable even at the lowest NK/DC ratio tested (1:5) indicating that NK-DC conjugates are formed in our other experiments measuring cytokine production and cell killing.\nOur initial experiments using resting NK cells (Fig. 1) demonstrated a contact-dependent NK effect driving iDCs to mature. Therefore, we tested what effects activated NK cells mediated on DC maturation (Fig. 4). Similar to our previous results with activated NK cells (Figs. 2 and 3), addition of NK cells to the culture leads to opposing effects on the iDC population depending on the NK/DC ratio. Compared with the untreated DCs (Fig. 4 A-C), low NK/DC ratios (1:5 or 1:1) consistently augmented expression of the maturation markers: CD86 (Fig. 4 D-I), CD83, and HLA-DR (data not shown). At a 5:1 ratio (NK/DC) most of the DCs are nonviable (Fig. 4 J-L). Addition of suboptimal doses of LPS (Fig. 4 C, F, I, and L) augmented the NK-induced maturation at NK/DC ratios of 1:5 and 1:1, but had no effect at the 5:1 ratio. Again, DC maturation was dependent on NK cell contact and endogenously produced TNF-alpha, because it did not occur when the two cell types were separated in trans-wells or upon the addition of a neutralizing antibody for TNF-alpha (Fig. 5). Moreover, addition of blocking reagents for CD80, CD86, CD154, CD95, CD11a, CD50, IL-12, IFN-gamma, IFN-alpha, or IFN-beta had no effect on the NK-induced maturation (data not shown).\nFigure 4.\nActivated/cultured NK cell-mediated maturation/death of DCs. Cultured iDCs were incubated for 48 h, alone (A-C), or with NK cells at the following ratios (NK/DC), 1:5 (D-F), 1:1 (G-I), and 5:1 (J-L). Forward versus side scatter plots (A, D, G, and J) show the gating on the DC subset and demonstrate its disappearance at the 5:1 (NK/DC) ratio (J). Propidium iodide staining of the NK/DC (5:1) cultures confirmed the almost complete absence of viable DCs (data not shown). Staining for CD86 expression was performed as described in Fig. 1 and the histograms are shown for DCs cultured in the presence (C, F, I, and L) or absence (B, E, H, and K) of 1 ng/ml of LPS. Results are representative of six experiments performed.\nFigure 5.\nActivated/cultured NK cell-induced DC maturation is dependent on cell-to-cell contact and endogenous TNF-alpha production. Cultured iDCs were incubated alone (A, D, and G); with activated NK cells at an NK/DC ratio of 1:5 (B, E, and H); with activated NK cells (NK/DC; 1:5) separated in trans-wells (C and F); or with activated NK cells and 10 mug/ml of a neutralizing antibody for TNF-alpha (I). LPS concentrations used were: 0 ng/ml (A-C); 10 ng/ml (D-F) and 50 ng/ml (G-I). CD86 staining of the DC subset was performed as in Figs. 1 and 4. Results are representative of four experiments performed.\n" ], "offsets": [ [ 0, 10597 ] ] } ]
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"normalized": [] }, { "id": "PMC-2193592-sec-11_T181", "type": "Cell", "text": [ "NK" ], "offsets": [ [ 10199, 10201 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T182", "type": "Cell", "text": [ "DC" ], "offsets": [ [ 10202, 10204 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T183", "type": "Cell", "text": [ "NK cells" ], "offsets": [ [ 10248, 10256 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T184", "type": "Cell", "text": [ "NK" ], "offsets": [ [ 10258, 10260 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T185", "type": "Cell", "text": [ "DC" ], "offsets": [ [ 10261, 10263 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T186", "type": "Cell", "text": [ "NK cells" ], "offsets": [ [ 10324, 10332 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T187", "type": "Cell", "text": [ "DC" ], "offsets": [ [ 10494, 10496 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T188", "type": "Tissue", "text": [ "tissues" ], "offsets": [ [ 671, 678 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T189", "type": "Cell", "text": [ "NK cells" ], "offsets": [ [ 7632, 7640 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T190", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 7645, 7650 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T191", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 2356, 2361 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T192", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 2649, 2654 ] ], "normalized": [] }, { "id": "PMC-2193592-sec-11_T193", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 7994, 7998 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2989791-sec-04
PMC-2989791-sec-04
[ { "id": "PMC-2989791-sec-04__text", "type": "sec", "text": [ "Measurement of IgA1 content\nIgA1 content in the supernatant from each culture well was measured in duplicate using enzyme-linked immunosorbent assay (ELISA). All incubations were performed at room temperature except for capture antibody coating. Briefly, 96-well immunoplates (Thermo Fisher Scientific, Waltham, MA, USA) were coated with 5 microg/mL of F(ab')2 fragment goat anti-human IgA antibody (Jackson ImmunoResearch Laboratories, West Grove, PA, USA), in phosphate-buffered saline (PBS) at 4degreesC overnight. After three washes with PBS containing 0.05% Tween-20 (PBST), plates were blocked by adding PBS containing 1% bovine serum albumin (BSA) to the wells for 90 min. Next, 50 microL of supernatant sample or standard human IgA1 (CALBIOCHEM, La Jolla, CA, USA) was added to the reaction wells and then incubated for 90 min. After three washes, 0.75 microg/mL alkaline phosphatase conjugated goat anti-human IgA (Southern Biotechnology Associates, Birmingham, AL, USA) in 1% BSA/PBS was added to the reaction wells and then incubated for 90 min. Plates were washed three times and developed with a substrate solution of 1 mg/mL p-nitrophenyl phosphate disodium salt (SIGMA, St. Louis, MO, USA) in 0.1 M glycine buffer containing 1 mM MgCl2, 1 mM ZnCl2, pH 10.4. The optical density at 405 nm was determined in a microplate reader (Benchmark PlusTM Bio-Rad Laboratories, Hercules, CA, USA). IgA1 concentration in unknown duplicate samples was determined by interpolation of the respective optical density into the appropriate standard curve. IgG and IgM contents in the supernatant were measured using sandwich ELISA (IMMUNOtek(R), ZeptoMetrix Corporation, Buffalo, NY, USA) according to the manufacturer's instructions.\n" ], "offsets": [ [ 0, 1731 ] ] } ]
[ { "id": "PMC-2989791-sec-04_T1", "type": "Organism_substance", "text": [ "supernatant" ], "offsets": [ [ 48, 59 ] ], "normalized": [] }, { "id": "PMC-2989791-sec-04_T2", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 635, 640 ] ], "normalized": [] }, { "id": "PMC-2989791-sec-04_T4", "type": "Organism_substance", "text": [ "supernatant sample" ], "offsets": [ [ 699, 717 ] ], "normalized": [] }, { "id": "PMC-2989791-sec-04_T5", "type": "Organism_substance", "text": [ "supernatant" ], "offsets": [ [ 1580, 1591 ] ], "normalized": [] } ]
[]
[]
[]
PMID-12604762
PMID-12604762
[ { "id": "PMID-12604762__text", "type": "abstract", "text": [ "Rural/urban differences in access to and utilization of services among people in Alabama with sickle cell disease.\nOBJECTIVE:\nThis study examined relationships between socioeconomic factors and the geographic distribution of 662 cases of sickle cell disease in Alabama in 1999-2001.\nMETHODS:\nMeasures of community distress, physical functioning, and medical problems were used in analyzing utilization differences between individuals with sickle cell disease living in urban and rural areas.\nRESULTS:\nUtilization of comprehensive sickle cells disease services was lower for individuals with sickle cell disease living in rural areas than for those living in urban areas. Rural clients reported significantly more limitations than urban clients on several measures of physical functioning. The results also suggest that utilization of services was higher for those with more medical problems and those who lived in high distress areas, although these findings did not meet the criterion for statistical significance.\nCONCLUSIONS:\nConclusions based on statistical evidence that geographic location and socioeconomic factors relate to significantly different health care service experience bear important implications for medical and health care support systems, especially on the community level.\n" ], "offsets": [ [ 0, 1295 ] ] } ]
[ { "id": "PMID-12604762_T1", "type": "Cell", "text": [ "sickle cell" ], "offsets": [ [ 94, 105 ] ], "normalized": [] }, { "id": "PMID-12604762_T2", "type": "Cell", "text": [ "sickle cell" ], "offsets": [ [ 238, 249 ] ], "normalized": [] }, { "id": "PMID-12604762_T3", "type": "Cell", "text": [ "sickle cell" ], "offsets": [ [ 439, 450 ] ], "normalized": [] }, { "id": "PMID-12604762_T4", "type": "Cell", "text": [ "sickle cells" ], "offsets": [ [ 530, 542 ] ], "normalized": [] }, { "id": "PMID-12604762_T5", "type": "Cell", "text": [ "sickle cell" ], "offsets": [ [ 591, 602 ] ], "normalized": [] } ]
[]
[]
[]
PMID-14714614
PMID-14714614
[ { "id": "PMID-14714614__text", "type": "abstract", "text": [ "Prognostic significance and correlation with survival of bcl-2 and TGF-beta RII in colon cancer.\nBcl-2 and TGF-beta receptors type II (RII) in colon carcinomas were studied in a series of 113 patients, to determine their prognostic significance and to correlate their expression with other prognostic indicators. Bcl-2 expression in the tumor cells showed a reverse relation with tumor size (P = 0.018), histological grade (P = 0.04), and stage (P = 0.013). Univariate survival analysis using the log rank test showed that the survival of patients with bcl-2-positive tumors was significantly better than the survival of patients with bcl-2-negative tumors (P = 0.02). However, when entered into a multivariate analysis model, it was not found to be of independent prognostic significance. TGF-beta RII expression was correlated with stage (P = 0.03), while no statistically significant correlation was found between TGF-beta RII expression and histological grade or survival. In conclusion, these results provide additional evidence for the role of bcl-2 and TGF-beta RII in carcinogenesis of the colon, while they do not support the use of these factors as prognostic markers in patients with colon cancer.\n" ], "offsets": [ [ 0, 1209 ] ] } ]
[ { "id": "PMID-14714614_T1", "type": "Pathological_formation", "text": [ "colon cancer" ], "offsets": [ [ 83, 95 ] ], "normalized": [] }, { "id": "PMID-14714614_T2", "type": "Pathological_formation", "text": [ "colon carcinomas" ], "offsets": [ [ 143, 159 ] ], "normalized": [] }, { "id": "PMID-14714614_T3", "type": "Cell", "text": [ "tumor cells" ], "offsets": [ [ 337, 348 ] ], "normalized": [] }, { "id": "PMID-14714614_T4", "type": "Pathological_formation", "text": [ "tumor" ], "offsets": [ [ 380, 385 ] ], "normalized": [] }, { "id": "PMID-14714614_T5", "type": "Pathological_formation", "text": [ "bcl-2-positive tumors" ], "offsets": [ [ 553, 574 ] ], "normalized": [] }, { "id": "PMID-14714614_T6", "type": "Pathological_formation", "text": [ "bcl-2-negative tumors" ], "offsets": [ [ 635, 656 ] ], "normalized": [] }, { "id": "PMID-14714614_T7", "type": "Organ", "text": [ "colon" ], "offsets": [ [ 1098, 1103 ] ], "normalized": [] }, { "id": "PMID-14714614_T8", "type": "Pathological_formation", "text": [ "colon cancer" ], "offsets": [ [ 1195, 1207 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2660343-sec-18
PMC-2660343-sec-18
[ { "id": "PMC-2660343-sec-18__text", "type": "sec", "text": [ "Peptide-BSA conjugates as diagnostic antigens\nTo analyse the potential of the peptides to behave as antigen mimics, their ability to react with IgM antibodies from individuals infected with EBV was assessed. In our previous study, we demonstrated that the sensitivity of detection was greatly improved when the peptides were coupled to a carrier molecule such as BSA prior to immobilisation onto a solid surface (Casey et al., 2006). This strategy was adopted to test peptides Eb1-4 and H1. A set of 40 clinical samples that were classified as EBV seropositive (n = 16), seronegative (n = 16) or potentially cross-reactive sera (n = 8) were assessed for reactivity with Eb1-4 and H1 peptides individually. The cut-off level was defined as the mean optical density of the seronegative samples plus 3 standard deviations shown as a line on the graphs in Fig. 5. Readings above this level were defined as positive and below this level negative. The same set of samples were analysed on BSA alone and these values were subtracted from the peptide-BSA conjugate readings and the corrected absorbance readings were plotted individually for our new peptides Eb1-4 and H1 in Fig. 5. There was a clear difference in the detection of seropositive antibodies by all the peptides (Fig. 5A-E) compared with the analysis of BSA alone (Fig. 5F), with the majority of absorbance readings above the cut-off level. We compared the ability of our panel of peptide mimotopes to be recognised by antibodies in the same set of seropositive samples in Fig. 6A and the sensitivity of detection is shown in Fig. 6B. We also included F1 and Gp125 mimotopes specific for two mAbs in our previous study (Casey et al., 2006). Of the peptides identified from polyclonal sera Eb1, Gp125 and F1 had the highest sensitivity (94%). Slightly lower sensitivity was observed for Eb2, 3 and 4 (88%) and H1 peptide had the lowest sensitivity (81%) as summarised in Fig. 6B. The sensitivity of F1 and Gp125 was similar to that produced by the mimotopes selected in our previous study, 95% for F1 and 92% for Gp125.\nFig. 5\nEvaluation of peptides Eb1-4 and H1 coupled to BSA as EBV diagnostic reagents. Human serum (n = 40) previously analysed using a diagnostic test for VCA IgM was allowed to react with the peptides and the bound IgM antibodies were detected using anti-human IgM HRP. The absorbance readings for 1 (positive), 2 (negative) and putative cross-reactive sera for 3 (Parvo), 4 (HSV), 5 (CMV) and 6 (RF) are plotted for (A) Eb1, (B) Eb2, (C) Eb3, (D) Eb4, (E) H1 and (F) BSA, respectively. The cut-off value is defined as the mean of the negative population +3SD indicated by a solid horizontal line; since there were no false positives, the specificity for each mimotope was 100%.\nFig. 6\nComparison of the reactivities of our panel of mimotopes Eb1-4, H1, F1 and Gp125 conjugated to BSA with EBV IgM-positive sera (n = 16) absorbance values are plotted and the cut-off levels are depicted by a horizontal line in (A). (B) Summary of the false-negative results from the 5/16 serum samples seropositive for IgM EBV and the overall sensitivity for each mimotope for diagnosis of EBV IgM antibodies.\nWe also considered which seropositive EBV samples contained antibodies that did not recognise the panel of peptides, i.e. false-negative readings, listed in Fig. 6B. The antibodies in serum 1 (s1) were unreactive with all of the peptides identified in this study, s2 was not reactive with Eb3, Eb4 and H1 and s3 was unreactive with H1. Gp125 and F1 that were selected in our previous study were recognised by s1, 2 and 3; however, two different serum samples (s4 and 5) did not recognise F1 or Gp125, respectively. This demonstrates that individual peptides are not recognised by all EBV antibodies and confirms that different peptides are required to represent different epitopes. Therefore, a combination of Eb1 peptide F1 and Gp125 peptides could be recognised by antibodies present in all this set of EBV clinical samples resulting in 100% sensitivity.\nFor the samples defined as EBV-seronegative, there were no readings above the cut-off level and therefore no false positives, resulting in 100% specificity. In addition, there were no absorbance readings above the cut-off levels for the potentially cross-reactive serum samples, inferring that the peptides identified in this study have high specificity for EBV antibodies.\n" ], "offsets": [ [ 0, 4401 ] ] } ]
[ { "id": "PMC-2660343-sec-18_T1", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 1740, 1744 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T2", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 2167, 2172 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T3", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 2429, 2433 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T4", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 2883, 2887 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T5", "type": "Organism_substance", "text": [ "serum samples" ], "offsets": [ [ 3048, 3061 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T6", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 3354, 3359 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T7", "type": "Organism_substance", "text": [ "serum samples" ], "offsets": [ [ 3615, 3628 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T8", "type": "Organism_substance", "text": [ "serum samples" ], "offsets": [ [ 4291, 4304 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T9", "type": "Organism_substance", "text": [ "samples" ], "offsets": [ [ 3212, 3219 ] ], "normalized": [] }, { "id": "PMC-2660343-sec-18_T14", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 623, 627 ] ], "normalized": [] } ]
[]
[]
[]
PMC-1557851-sec-01
PMC-1557851-sec-01
[ { "id": "PMC-1557851-sec-01__text", "type": "sec", "text": [ "Background\nHallucinations may occur in any sensory modalities. Formed musical hallucinations (i.e. Perception of either vocal or instrumental melodies) reported in English literature to date have typically been associated with marked hearing loss, advanced age, female sex (71%), lack of response to treatment and associated psychopathology [1] but has been concluded that hearing loss is neither a necessary nor sufficient condition for the occurrence of musical hallucinations [1]. Tumor like Astrocytoma, Temporal lobe epilepsy, raised intra cranial tension, drug induced (tricyclics, Propronolol etc ;), meningitis and psychotic illness were shown to cause palinacousis and musical hallucinations [2,3].\nMusical hallucinations are pseudo hallucinations that originate in memory representations and they may undergo a transition to true hallucination. In musical hallucination spatial projection is less definite. Sometimes they are perceived like the tinnitus in patient's own head. The quality is usually very intense and distinct often very loud. They vary from elementary sounds to instrumental music, vocal music, bird songs, bells, pieces of melodies or sentences, religious music etc:- We report an unusual presentation of an elderly lady who had experienced musical hallucinations whilst being treated with Electro Convulsive Therapy. Though this has never been reported earlier, there seemed to have a good association between the initiation of Electro convulsive therapy and musical hallucination in our patient.\n" ], "offsets": [ [ 0, 1526 ] ] } ]
[ { "id": "PMC-1557851-sec-01_T1", "type": "Pathological_formation", "text": [ "Tumor" ], "offsets": [ [ 484, 489 ] ], "normalized": [] }, { "id": "PMC-1557851-sec-01_T2", "type": "Pathological_formation", "text": [ "Astrocytoma" ], "offsets": [ [ 495, 506 ] ], "normalized": [] }, { "id": "PMC-1557851-sec-01_T3", "type": "Multi-tissue_structure", "text": [ "Temporal lobe" ], "offsets": [ [ 508, 521 ] ], "normalized": [] }, { "id": "PMC-1557851-sec-01_T4", "type": "Organism_subdivision", "text": [ "cranial" ], "offsets": [ [ 545, 552 ] ], "normalized": [] }, { "id": "PMC-1557851-sec-01_T5", "type": "Organism_subdivision", "text": [ "head" ], "offsets": [ [ 981, 985 ] ], "normalized": [] } ]
[]
[]
[]
PMC-1281295-caption-02
PMC-1281295-caption-02
[ { "id": "PMC-1281295-caption-02__text", "type": "caption", "text": [ "Measured analytes in five biologic sample matrices.a\n" ], "offsets": [ [ 0, 53 ] ] } ]
[]
[]
[]
[]
PMID-19269647
PMID-19269647
[ { "id": "PMID-19269647__text", "type": "abstract", "text": [ "Handling within run retention time shifts in two-dimensional chromatography data using shift correction and modeling.\nThe use of PARAFAC for modeling GC x GC-TOFMS peaks is well documented. This success is due to the trilinear structure of these data under ideal, or sufficiently close to ideal, chromatographic conditions. However, using temperature programming to cope with the general elution problem, deviations from trilinearity within a run are more likely to be seen for the following three cases: (1) compounds (i.e., analytes) severely broadened on the first column hence defined by many modulation periods, (2) analytes with a very high retention factor on the second column and likely wrapped around in that dimension, or (3) with fast temperature program rates. This deviation from trilinearity is seen as retention time-shifted peak profiles in subsequent modulation periods (first column fractions). In this report, a relaxed yet powerful version of PARAFAC, known as PARAFAC2 has been applied to handle this shift within the model step by allowing generation of individual peak profiles in subsequent first column fractions. An alternative approach was also studied, utilizing a standard retention time shift correction to restore the data trilinearity structure followed by PARAFAC. These two approaches are compared when identifying and quantifying a known analyte over a large concentration series where a certain shift is simulated in the successive first column fractions. Finally, the methods are applied to real chromatographic data showing severely shifted peak profiles. The pros and cons of the presented approaches are discussed in relation to the model parameters, the signal-to-noise ratio and the degree of shift.\n" ], "offsets": [ [ 0, 1743 ] ] } ]
[]
[]
[]
[]
PMC-2578989-sec-01
PMC-2578989-sec-01
[ { "id": "PMC-2578989-sec-01__text", "type": "sec", "text": [ "Images\nFigure 1\nFigure 5\nFigure 6\n" ], "offsets": [ [ 0, 34 ] ] } ]
[]
[]
[]
[]
PMID-18578357
PMID-18578357
[ { "id": "PMID-18578357__text", "type": "abstract", "text": [ "Intraoperative handling and wound healing of arthroscopic portal wounds: a clinical study comparing nylon suture with wound closure strips.\nThis prospective, single-centre study compared wound closure methods in patients undergoing arthroscopy. Closure of arthroscopic portal wounds with sterile adhesive strips is effective and convenient for wound management. The method was associated with a reduced potential for infection, faster renewal of tensile strength, greater cost effectiveness, and better cosmetic effects comparing with suture closure. This method of wound closure may also reduce the incidence of needle stick injury in the theatre environment. Thereby the incidence of percutaneous exposure following a surgical procedure may not facilitate transmission of blood borne pathogens such as human immunodeficiency virus (HIV), hepatitis C virus and hepatitis B virus. As a result it may reduce litigation in today's changing healthcare climate.\n" ], "offsets": [ [ 0, 958 ] ] } ]
[ { "id": "PMID-18578357_T1", "type": "Pathological_formation", "text": [ "wound" ], "offsets": [ [ 28, 33 ] ], "normalized": [] }, { "id": "PMID-18578357_T2", "type": "Pathological_formation", "text": [ "wounds" ], "offsets": [ [ 65, 71 ] ], "normalized": [] }, { "id": "PMID-18578357_T3", "type": "Pathological_formation", "text": [ "wound" ], "offsets": [ [ 118, 123 ] ], "normalized": [] }, { "id": "PMID-18578357_T4", "type": "Pathological_formation", "text": [ "wound" ], "offsets": [ [ 187, 192 ] ], "normalized": [] }, { "id": "PMID-18578357_T5", "type": "Pathological_formation", "text": [ "wounds" ], "offsets": [ [ 276, 282 ] ], "normalized": [] }, { "id": "PMID-18578357_T6", "type": "Pathological_formation", "text": [ "wound" ], "offsets": [ [ 344, 349 ] ], "normalized": [] }, { "id": "PMID-18578357_T7", "type": "Pathological_formation", "text": [ "wound" ], "offsets": [ [ 566, 571 ] ], "normalized": [] }, { "id": "PMID-18578357_T8", "type": "Organism_substance", "text": [ "blood" ], "offsets": [ [ 774, 779 ] ], "normalized": [] } ]
[]
[]
[]
PMID-12476350
PMID-12476350
[ { "id": "PMID-12476350__text", "type": "abstract", "text": [ "CXC chemokine receptors in the central nervous system: Role in cerebellar neuromodulation and development.\nChemokines and their receptors are constitutively present in the central nervous system (CNS), expressed in neurons and glial cells. Much evidence suggests that, beyond their involvement in neuroinflammation, these proteins play a role in neurodevelopment and neurophysiological signaling. The goal of this review is to summarize recent information concerning expression, signaling, and function of CXC chemokine receptor in the CNS, with the main focus on the developmental and neuromodulatory actions of chemokines in the cerebellum.\n" ], "offsets": [ [ 0, 643 ] ] } ]
[ { "id": "PMID-12476350_T1", "type": "Anatomical_system", "text": [ "central nervous system" ], "offsets": [ [ 31, 53 ] ], "normalized": [] }, { "id": "PMID-12476350_T2", "type": "Multi-tissue_structure", "text": [ "cerebellar" ], "offsets": [ [ 63, 73 ] ], "normalized": [] }, { "id": "PMID-12476350_T3", "type": "Anatomical_system", "text": [ "central nervous system" ], "offsets": [ [ 172, 194 ] ], "normalized": [] }, { "id": "PMID-12476350_T4", "type": "Anatomical_system", "text": [ "CNS" ], "offsets": [ [ 196, 199 ] ], "normalized": [] }, { "id": "PMID-12476350_T5", "type": "Cell", "text": [ "neurons" ], "offsets": [ [ 215, 222 ] ], "normalized": [] }, { "id": "PMID-12476350_T6", "type": "Cell", "text": [ "glial cells" ], "offsets": [ [ 227, 238 ] ], "normalized": [] }, { "id": "PMID-12476350_T7", "type": "Multi-tissue_structure", "text": [ "cerebellum" ], "offsets": [ [ 631, 641 ] ], "normalized": [] }, { "id": "PMID-12476350_T8", "type": "Anatomical_system", "text": [ "CNS" ], "offsets": [ [ 536, 539 ] ], "normalized": [] } ]
[]
[ { "id": "PMID-12476350_1", "entity_ids": [ "PMID-12476350_T3", "PMID-12476350_T4" ] } ]
[]
PMID-9380745
PMID-9380745
[ { "id": "PMID-9380745__text", "type": "abstract", "text": [ "Blind separation of auditory event-related brain responses into independent components.\nAveraged event-related potential (ERP) data recorded from the human scalp reveal electroencephalographic (EEG) activity that is reliably time-locked and phase-locked to experimental events. We report here the application of a method based on information theory that decomposes one or more ERPs recorded at multiple scalp sensors into a sum of components with fixed scalp distributions and sparsely activated, maximally independent time courses. Independent component analysis (ICA) decomposes ERP data into a number of components equal to the number of sensors. The derived components have distinct but not necessarily orthogonal scalp projections. Unlike dipole-fitting methods, the algorithm does not model the locations of their generators in the head. Unlike methods that remove second-order correlations, such as principal component analysis (PCA), ICA also minimizes higher-order dependencies. Applied to detected-and undetected-target ERPs from an auditory vigilance experiment, the algorithm derived ten components that decomposed each of the major response peaks into one or more ICA components with relatively simple scalp distributions. Three of these components were active only when the subject detected the targets, three other components only when the target went undetected, and one in both cases. Three additional components accounted for the steady-state brain response to a 39-Hz background click train. Major features of the decomposition proved robust across sessions and changes in sensor number and placement. This method of ERP analysis can be used to compare responses from multiple stimuli, task conditions, and subject states.\n" ], "offsets": [ [ 0, 1742 ] ] } ]
[ { "id": "PMID-9380745_T1", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 43, 48 ] ], "normalized": [] }, { "id": "PMID-9380745_T2", "type": "Multi-tissue_structure", "text": [ "scalp" ], "offsets": [ [ 156, 161 ] ], "normalized": [] }, { "id": "PMID-9380745_T3", "type": "Multi-tissue_structure", "text": [ "scalp" ], "offsets": [ [ 403, 408 ] ], "normalized": [] }, { "id": "PMID-9380745_T4", "type": "Multi-tissue_structure", "text": [ "scalp" ], "offsets": [ [ 453, 458 ] ], "normalized": [] }, { "id": "PMID-9380745_T5", "type": "Multi-tissue_structure", "text": [ "scalp" ], "offsets": [ [ 718, 723 ] ], "normalized": [] }, { "id": "PMID-9380745_T6", "type": "Organism_subdivision", "text": [ "head" ], "offsets": [ [ 838, 842 ] ], "normalized": [] }, { "id": "PMID-9380745_T7", "type": "Multi-tissue_structure", "text": [ "scalp" ], "offsets": [ [ 1215, 1220 ] ], "normalized": [] }, { "id": "PMID-9380745_T8", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 1461, 1466 ] ], "normalized": [] } ]
[]
[]
[]
PMID-8102531
PMID-8102531
[ { "id": "PMID-8102531__text", "type": "abstract", "text": [ "Epilepsy in Down syndrome: clinical aspects and possible mechanisms.\nAlthough epilepsy is more common in persons with trisomy 21 (Down syndrome) than in the general population, the mechanisms by which seizures are generated in this population have received little attention. It is likely that this increased seizure susceptibility is due to a combination of medical risk factors and inherent neurologic abnormalities characteristic of Down syndrome. In this review clinical aspects of seizures among individuals with Down syndrome were described and possible mechanisms by which the trisomy 21 brain may generate seizures were explored.\n" ], "offsets": [ [ 0, 637 ] ] } ]
[ { "id": "PMID-8102531_T1", "type": "Anatomical_system", "text": [ "neurologic" ], "offsets": [ [ 392, 402 ] ], "normalized": [] }, { "id": "PMID-8102531_T2", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 594, 599 ] ], "normalized": [] } ]
[]
[]
[]
PMID-16252749
PMID-16252749
[ { "id": "PMID-16252749__text", "type": "abstract", "text": [ "Sensitivity variation in two-center holographic recording.\nAn experimental study of variation of sensitivity with recording and sensitizing intensities in two-center recording is presented. The experimental results are in good agreement with the theoretical predictions. It is shown experimentally, for what is to our knowledge the first time, that the sensitivity is a function of the ratio of recording to sensitizing intensities and not the absolute intensities. Also, the ratio of recording to sensitizing intensities should be small to obtain high sensitivity values. We also report the highest sensitivity (S=0.15 cm/J) that has been achieved to date for a LiNbO3:Fe:Mn crystal.\n" ], "offsets": [ [ 0, 685 ] ] } ]
[]
[]
[]
[]
PMC-1072800-sec-07
PMC-1072800-sec-07
[ { "id": "PMC-1072800-sec-07__text", "type": "sec", "text": [ "Immunostaining and confocal analysis\nDNA labelling and staining with 5-bromo-2'-deoxyuridine (BrdU labelling and detection kit I; Boehringer Mannheim, Germany) was performed according to the manufacturer's instructions. The nucleoli were detected with an anti-nucleolin antibody (clone 3G4B2; Upstate biotechnology, Lake Placid, NY) on cells fixed in 2% formalin for 10 min followed by permeabilization with ice-cold methanol for 30 min. The secondary antibody used for both BrdU and nucleoli staining was a rhodamine (tetra-methyl)-conjugated goat anti-mouse antibody (T-2762) from Molecular Probe (Eugene, OR). The cells were examined in a Zeiss LSM 510 laser scanning microscope equipped with a Plan-Apochromate 63x/1.4 oil immersion objective. We used the 488 nm laser line for excitation of EGFP (detected at 505 nm < lambdaEGFP < 530 nm) and the 543 nm laser line for rhodamine (tetra-methyl) (detected at lambdaRhodamine > 560 nm). ECFP fusion protein was excited with a 458 nm laser line (detected at 480 nm < lambdaECFP < 520 nm), EYFP fusion protein was excited with a 514 nm laser line (lambdaEGFP > 560 nm) and HcRed fusion protein was excited with a 543 nm laser line and detected at >585 or 650 nm. The images were from 1 mum thick slices of the cells. The images were exported into Adobe Photoshop (Adobe Systems Inc., San Jose, CA).\n" ], "offsets": [ [ 0, 1349 ] ] } ]
[ { "id": "PMC-1072800-sec-07_T1", "type": "Cellular_component", "text": [ "nucleoli" ], "offsets": [ [ 224, 232 ] ], "normalized": [] }, { "id": "PMC-1072800-sec-07_T2", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 336, 341 ] ], "normalized": [] }, { "id": "PMC-1072800-sec-07_T3", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 617, 622 ] ], "normalized": [] }, { "id": "PMC-1072800-sec-07_T4", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 1260, 1265 ] ], "normalized": [] }, { "id": "PMC-1072800-sec-07_T6", "type": "Cellular_component", "text": [ "nucleoli" ], "offsets": [ [ 484, 492 ] ], "normalized": [] }, { "id": "PMC-1072800-sec-07_T7", "type": "Cell", "text": [ "slices" ], "offsets": [ [ 1246, 1252 ] ], "normalized": [] } ]
[]
[]
[ { "id": "PMC-1072800-sec-07_R1", "type": "Part-of", "arg1_id": "PMC-1072800-sec-07_T7", "arg2_id": "PMC-1072800-sec-07_T4", "normalized": [] } ]
PMID-11716301
PMID-11716301
[ { "id": "PMID-11716301__text", "type": "abstract", "text": [ "Assembly strategies and GTPase regulation of the eukaryotic and Escherichia coil translocons.\nThe translocation of most proteins across the endoplasmic reticulum or bacterial inner membrane occurs through an aqueous pore that spans the membrane. Substrates that are translocated co-translationally across the membrane are directed to the translocation pore via an interaction between the cytosolic signal recognition particle and its membrane-bound receptor. Together the translocation pore and the receptor are referred to as a translocon. By studying the biogenesis of the translocon a number of alternate targeting and membrane-integration pathways have been discovered that operate independently of the signal recognition particle (SRP) pathway. The novel assembly strategies of the translocon and the ways in which these components interact to ensure the fidelity and unidirectionality of the targeting and translocation process are reviewed here.\n" ], "offsets": [ [ 0, 953 ] ] } ]
[ { "id": "PMID-11716301_T1", "type": "Cellular_component", "text": [ "endoplasmic reticulum" ], "offsets": [ [ 140, 161 ] ], "normalized": [] }, { "id": "PMID-11716301_T2", "type": "Cellular_component", "text": [ "inner membrane" ], "offsets": [ [ 175, 189 ] ], "normalized": [] }, { "id": "PMID-11716301_T4", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 236, 244 ] ], "normalized": [] }, { "id": "PMID-11716301_T5", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 309, 317 ] ], "normalized": [] }, { "id": "PMID-11716301_T6", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 434, 442 ] ], "normalized": [] }, { "id": "PMID-11716301_T7", "type": "Cellular_component", "text": [ "translocation pore" ], "offsets": [ [ 472, 490 ] ], "normalized": [] }, { "id": "PMID-11716301_T8", "type": "Cellular_component", "text": [ "translocation pore" ], "offsets": [ [ 338, 356 ] ], "normalized": [] }, { "id": "PMID-11716301_T9", "type": "Cellular_component", "text": [ "aqueous pore" ], "offsets": [ [ 208, 220 ] ], "normalized": [] }, { "id": "PMID-11716301_T10", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 622, 630 ] ], "normalized": [] }, { "id": "PMID-11716301_T3", "type": "Organism_substance", "text": [ "cytosolic" ], "offsets": [ [ 388, 397 ] ], "normalized": [] }, { "id": "PMID-11716301_T11", "type": "Cellular_component", "text": [ "translocon" ], "offsets": [ [ 529, 539 ] ], "normalized": [] }, { "id": "PMID-11716301_T12", "type": "Cellular_component", "text": [ "translocon" ], "offsets": [ [ 575, 585 ] ], "normalized": [] }, { "id": "PMID-11716301_T13", "type": "Cellular_component", "text": [ "translocon" ], "offsets": [ [ 787, 797 ] ], "normalized": [] }, { "id": "PMID-11716301_T14", "type": "Cellular_component", "text": [ "translocons" ], "offsets": [ [ 81, 92 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3003518-sec-05
PMC-3003518-sec-05
[ { "id": "PMC-3003518-sec-05__text", "type": "sec", "text": [ "Introduction\nAdipose tissue, once viewed as simply a storage and release depot for lipids, is now considered an endocrine tissue [1,2] that secretes various substances (adipokines), including tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, leptin, adiponectin, resistin, visfatin, and omenetin [3,4]. Among these adipokines, much attention has been paid to adiponectin's relationship with insulin sensitivity and glucose and lipid metabolism in the past 10 years. In addition, adiponectin is known to exhibit potent anti-inflammatory [5], atheroprotective [6], and antidiabetic [7] effects.\nRecent findings suggest that adiponectin may be involved in the pathogenesis of rheumatoid arthritis (RA). Levels of adiponectin in synovial fluid and sera were elevated in patients with RA [8,9]. Adiponectin also induces the production of proinflammatory cytokines, IL-6, matrix metalloproteinase (MMP)-1, and IL-8 from RA synovial fibroblasts in vitro [10,11]. Thus, it was suggested that adiponectin can also exert significant proinflammatory and matrix-degrading effects. However, the role of adiponectin in the pathogenesis of RA is still controversial because of conflicting reports about its function [10,12-15]. In particular, adiponectin seems to play an anti-inflammatory role because it significantly inhibited IL-1beta-stimulated synovial cell proliferation in collagen-induced arthritic mice, despite increased IL-6 expression [16]. In contrast, high-grade inflammation in RA patients was negatively correlated with circulating adiponectin concentrations [17]. Rather, it was suggested that circulating adiponectin may be involved in cardiovascular disease in RA patients. Although this contradiction was partly explained by the induction of tolerance to inflammatory stimuli by adiponectin [18], the pro- or anti-inflammatory effects of adiponectin on the pathogenesis of RA remain unknown.\nWith regard to adiponectin's proinflammatory effects, we wondered whether adiponectin might stimulate the production of vascular endothelial growth factor (VEGF) and MMPs as well as proinflammatory mediators like IL-1beta and TNF-alpha do. In this study, we investigated the stimulatory effect of adiponectin on the production of IL-6, IL-8, prostaglandin E2 (PGE2), VEGF, and MMPs. In addition, the correlation between adiponectin and VEGF or MMPs was investigated by measuring the levels of these three proteins in the joint fluid of patients with RA or osteoarthritis (OA).\n" ], "offsets": [ [ 0, 2486 ] ] } ]
[ { "id": "PMC-3003518-sec-05_T1", "type": "Tissue", "text": [ "Adipose tissue" ], "offsets": [ [ 13, 27 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T2", "type": "Tissue", "text": [ "endocrine tissue" ], "offsets": [ [ 112, 128 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T4", "type": "Organism_substance", "text": [ "synovial fluid" ], "offsets": [ [ 736, 750 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T5", "type": "Organism_substance", "text": [ "sera" ], "offsets": [ [ 755, 759 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T6", "type": "Cell", "text": [ "synovial fibroblasts" ], "offsets": [ [ 928, 948 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T7", "type": "Cell", "text": [ "synovial cell" ], "offsets": [ [ 1346, 1359 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T8", "type": "Multi-tissue_structure", "text": [ "cardiovascular" ], "offsets": [ [ 1651, 1665 ] ], "normalized": [] }, { "id": "PMC-3003518-sec-05_T10", "type": "Organism_substance", "text": [ "joint fluid" ], "offsets": [ [ 2430, 2441 ] ], "normalized": [] } ]
[]
[]
[]
PMID-16210037
PMID-16210037
[ { "id": "PMID-16210037__text", "type": "abstract", "text": [ "Pathogenesis of thrombosis in essential thrombocythemia and polycythemia vera: the role of neutrophils.\nThrombotic complications are frequently observed in patients with polycythemia vera (PV) and essential thrombocythemia (ET). Abnormalities of red blood cells and platelets arising from the clonal rearrangement of hematopoietic cells have been considered, although causal relationships between any of these specific abnormalities and thrombosis have not been clearly established. The involvement of neutrophils and macrophages, which participate in thrombosis and hemostasis, has been insufficiently explored in PV and ET. Persistent activation of circulating neutrophils was recently demonstrated in ET and PV patients, in parallel with an increase in plasma concentrations of endothelial damage-derived and prothrombotic substances. Other studies have explored whether the augmentation of adhesion of neutrophils may affect neutrophil/platelet interaction since a significant increase in circulating neutrophil/platelet aggregates is found in ET and PV. This review summarizes the current knowledge of the pathogenesis of thrombosis in PV and ET, with emphasis on the role of neutrophils in hemostasis and their possible involvement in the mechanisms of the acquired thrombophilia of these patients. Available data suggest that these hemostatic markers deserve to be included in prospective clinical studies aimed at identifying their predictive role in the vascular complications of patients with ET and PV.\n" ], "offsets": [ [ 0, 1514 ] ] } ]
[ { "id": "PMID-16210037_T1", "type": "Cell", "text": [ "neutrophils" ], "offsets": [ [ 91, 102 ] ], "normalized": [] }, { "id": "PMID-16210037_T2", "type": "Cell", "text": [ "red blood cells" ], "offsets": [ [ 246, 261 ] ], "normalized": [] }, { "id": "PMID-16210037_T3", "type": "Cell", "text": [ "platelets" ], "offsets": [ [ 266, 275 ] ], "normalized": [] }, { "id": "PMID-16210037_T4", "type": "Cell", "text": [ "hematopoietic cells" ], "offsets": [ [ 317, 336 ] ], "normalized": [] }, { "id": "PMID-16210037_T5", "type": "Cell", "text": [ "neutrophils" ], "offsets": [ [ 502, 513 ] ], "normalized": [] }, { "id": "PMID-16210037_T6", "type": "Cell", "text": [ "macrophages" ], "offsets": [ [ 518, 529 ] ], "normalized": [] }, { "id": "PMID-16210037_T7", "type": "Cell", "text": [ "neutrophils" ], "offsets": [ [ 663, 674 ] ], "normalized": [] }, { "id": "PMID-16210037_T8", "type": "Organism_substance", "text": [ "plasma" ], "offsets": [ [ 756, 762 ] ], "normalized": [] }, { "id": "PMID-16210037_T9", "type": "Tissue", "text": [ "endothelial" ], "offsets": [ [ 781, 792 ] ], "normalized": [] }, { "id": "PMID-16210037_T10", "type": "Cell", "text": [ "neutrophils" ], "offsets": [ [ 906, 917 ] ], "normalized": [] }, { "id": "PMID-16210037_T11", "type": "Cell", "text": [ "neutrophil" ], "offsets": [ [ 929, 939 ] ], "normalized": [] }, { "id": "PMID-16210037_T12", "type": "Cell", "text": [ "platelet" ], "offsets": [ [ 940, 948 ] ], "normalized": [] }, { "id": "PMID-16210037_T13", "type": "Cell", "text": [ "neutrophil" ], "offsets": [ [ 1005, 1015 ] ], "normalized": [] }, { "id": "PMID-16210037_T14", "type": "Cell", "text": [ "platelet" ], "offsets": [ [ 1016, 1024 ] ], "normalized": [] }, { "id": "PMID-16210037_T15", "type": "Cell", "text": [ "neutrophils" ], "offsets": [ [ 1181, 1192 ] ], "normalized": [] }, { "id": "PMID-16210037_T16", "type": "Multi-tissue_structure", "text": [ "vascular" ], "offsets": [ [ 1463, 1471 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2474682-caption-05
PMC-2474682-caption-05
[ { "id": "PMC-2474682-caption-05__text", "type": "caption", "text": [ "Summary of studies reporting comorbidities with diabetes.\n" ], "offsets": [ [ 0, 58 ] ] } ]
[]
[]
[]
[]
PMC-2790131-sec-02
PMC-2790131-sec-02
[ { "id": "PMC-2790131-sec-02__text", "type": "sec", "text": [ "Subjects and Methods\nABPM was conducted for 60 selected patients who had visited Sunlin Hospital between January 2008 and August 2008. Patients were classified into 3 groups; an obese group whose body mass index (BMI) was > the 95th percentile, an overweight group whose BMI was > the 85th percentile but less than the 95th percentile, and a normal group whose BMI was below the 85th percentile. Overall mean BP, day and night BP and BP load were measured by ABPM.\n" ], "offsets": [ [ 0, 465 ] ] } ]
[ { "id": "PMC-2790131-sec-02_T1", "type": "Organism_subdivision", "text": [ "body" ], "offsets": [ [ 196, 200 ] ], "normalized": [] } ]
[]
[]
[]
PMID-17617824
PMID-17617824
[ { "id": "PMID-17617824__text", "type": "abstract", "text": [ "Rapid mixing between old and new C pools in the canopy of mature forest trees.\nStable C isotope signals in plant tissues became a key tool in explaining growth responses to the environment. The technique is based on the fundamental assumption that the isotopic composition of a given unit of tissue (e.g. a tree ring) reflects the specific C uptake conditions in the leaf at a given time. Beyond the methodological implications of any deviation from this assumption, it is of physiological interest whether new C is transferred directly from sources (a photosynthesizing leaf) to structural sinks (e.g. adjacent stem tissue), or inherently passes through existing (mobile) C pools, which may be of variable (older) age. Here, we explore the fate of (13)C-labelled photosynthates in the crowns of a 30-35 m tall, mixed forest using a canopy crane. In all nine study species labelled C reached woody tissue within 2-9 h after labelling. Four months later, very small signals were left in branch wood of Tilia suggesting that low mixing of new, labelled C with old C had taken place. In contrast, signals in Fagus and Quercus had increased, indicating more intense mixing. This species-specific mixing of new with old C pools is likely to mask year- or season-specific linkages between tree ring formation and climate and has considerable implications for climate reconstruction using stable isotopes as proxies for past climatic conditions.\n" ], "offsets": [ [ 0, 1439 ] ] } ]
[ { "id": "PMID-17617824_T1", "type": "Tissue", "text": [ "tissues" ], "offsets": [ [ 113, 120 ] ], "normalized": [] }, { "id": "PMID-17617824_T2", "type": "Tissue", "text": [ "tissue" ], "offsets": [ [ 292, 298 ] ], "normalized": [] }, { "id": "PMID-17617824_T3", "type": "Tissue", "text": [ "tree ring" ], "offsets": [ [ 307, 316 ] ], "normalized": [] }, { "id": "PMID-17617824_T4", "type": "Organ", "text": [ "leaf" ], "offsets": [ [ 367, 371 ] ], "normalized": [] }, { "id": "PMID-17617824_T5", "type": "Organ", "text": [ "leaf" ], "offsets": [ [ 571, 575 ] ], "normalized": [] }, { "id": "PMID-17617824_T6", "type": "Tissue", "text": [ "stem tissue" ], "offsets": [ [ 612, 623 ] ], "normalized": [] }, { "id": "PMID-17617824_T7", "type": "Organism_subdivision", "text": [ "crowns" ], "offsets": [ [ 786, 792 ] ], "normalized": [] }, { "id": "PMID-17617824_T8", "type": "Tissue", "text": [ "woody tissue" ], "offsets": [ [ 892, 904 ] ], "normalized": [] }, { "id": "PMID-17617824_T9", "type": "Tissue", "text": [ "tree ring" ], "offsets": [ [ 1283, 1292 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3274927-sec-07
PMC-3274927-sec-07
[ { "id": "PMC-3274927-sec-07__text", "type": "sec", "text": [ "Supplementary Material\nCrystal structure: contains datablock(s) global, I. DOI: 10.1107/S1600536812002796/hg5166sup1.cif\nStructure factors: contains datablock(s) I. DOI: 10.1107/S1600536812002796/hg5166Isup2.hkl\nAdditional supplementary materials: crystallographic information; 3D view; checkCIF report\n" ], "offsets": [ [ 0, 303 ] ] } ]
[]
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[]
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PMC-2858094-sec-14
PMC-2858094-sec-14
[ { "id": "PMC-2858094-sec-14__text", "type": "sec", "text": [ "Calcium intake and effects on QUS T-score\nFigure 5 shows the amounts of dietary calcium intake according to menopausal status. Calcium consumption in most groups, like that in the study population as a whole, was inadequate. Fewer than one third of premenopausal and postmenopausal women received more than 800 mg calcium daily, and fewer than 16% of premenopausal women in the 50-59 age decade (n = 38) consumed more than 800 mg calcium daily.\nFigure 5\nDaily calcium intake in premenopausal and postmenopausal women. This figure depicts the daily amounts of dietary calcium intake (and percent) according to menopausal status using 800 mg daily as cut off point.\nQUS T-score were then calculated according to daily calcium intake in all premenopausal and postmenopausal activity groups using 800 mg daily calcium as cutoff point. As shown in Tables 3 and 4 and Figure 6, premenopausal women who were systematically active and consumed more than 800 mg calcium daily had significantly higher QUS T-scores compared with all other activity groups (p < 0.05). Among systematically active premenopausal women who received more than 800 mg calcium per day, this difference was separately significant verses sedentary (p = 0.028) and moderately active (p = 0.04) women. In contrast, postmenopausal women showed no difference in QUS T-scores regardless of the amount of daily calcium intake.\nFigure 6\nSynergy between physical activity and dietary calcium intake in women consuming calcium amounts greater than 800 mg/day. This graphic depicts mean QUS T-score values calculated according to daily calcium intake in all premenopausal and postmenopausal activity groups using 800 mg daily as cut off point (for statistical significant values see text).\n" ], "offsets": [ [ 0, 1744 ] ] } ]
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PMID-1877751
PMID-1877751
[ { "id": "PMID-1877751__text", "type": "abstract", "text": [ "Quantitative retention-biological activity relationship study by micellar liquid chromatography.\nIn a previous paper, the usefulness of micellar liquid chromatography (MLC) in predicting octanol-water partition coefficients of organic compounds was reported. This paper is the first successful report of a quantitative retention-activity relationship study using the retention factor in MLC for predicting the biological activity of a group of phenolic compounds. Excellent correlation was obtained between the capacity factor in MLC and the bioactivity (measured as log 1/C, where C is the 50% inhibitory growth concentration) of 26 para-substituted phenols. A single MLC retention parameter is capable of describing the bioactivity of phenols, while three conventional molecular descriptors (log P(ow), pKa, and R) are needed to achieve a similar correlation. This indicates that both hydrophobic and electronic interactions are incorporated in a single MLC retention parameter, which is due to the amphiphilic nature of surfactants in the system. In situations like this, QRAR is a suitable alternative to QSAR since measuring MLC retention is much easier than measuring different molecular descriptors needed to build the QSAR model. Addition of 10% 2-propanol to a micellar system (hybrid system) proved to be the best chromatographic system for the best estimation of the phenols bioactivity. Other chromatographic factors such as pH and stationary phase also showed significant effect on the correlation between capacity factor k' and log 1/C.\n" ], "offsets": [ [ 0, 1551 ] ] } ]
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[]
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PMID-6229539
PMID-6229539
[ { "id": "PMID-6229539__text", "type": "abstract", "text": [ "Phosphorylation-induced mobility shift in phospholamban in sodium dodecyl sulfate-polyacrylamide gels. Evidence for a protein structure consisting of multiple identical phosphorylatable subunits.\nPhosphorylation of purified phospholamban isolated from canine cardiac sarcoplasmic reticulum vesicles decreased the electrophoretic mobility of the protein in sodium dodecyl sulfate (SDS)-polyacrylamide gels. Different mobility forms of phospholamban in SDS gels were visualized both by direct protein staining and by autoradiography. Unphosphorylated phospholamban migrated with an apparent Mr = 25,000 in SDS gels; maximal phosphorylation of phospholamban by cAMP- or Ca2+-calmodulin-dependent protein kinase increased the apparent Mr to 27,000. Partial phosphorylation of phospholamban by either protein kinase gave intermediate mobility forms of molecular weights between 25,000 and 27,000, suggesting that more than one phosphorylation site was present on the holoprotein for each activity. Boiling of phospholamban in SDS dissociated the holoprotein into an apparently homogeneous class of low molecular weight \"monomers.\" Only two mobility forms of monomeric phospholamban were observed in SDS gels after phosphorylation by cAMP-dependent protein kinase, corresponding to 9-kDa dephospho- and 11-kDa phosphoproteins. All of the 9-kDa protein could be phosphorylated and converted into the 11-kDa mobility form, suggesting the presence of only one site of phosphorylation on a single type of monomer for cAMP-dependent protein kinase. Simultaneous phosphorylation of monomeric phospholamban by cAMP-dependent protein kinase and Ca2+-calmodulin-dependent protein kinase gave an additional mobility form of the protein, suggesting that different sites of phosphorylation were present for each activity on each monomer. Incomplete dissociation of the holoprotein by boiling it in a relatively low concentration of SDS facilitated the detection of five major mobility forms of the protein in SDS gels, and the mobilities of all of these forms were decreased by phosphorylation. We propose that the high molecular weight form of phospholamban is a multimer of electrophoretically indistinguishable monomers, each of which contains a different phosphorylation site for cAMP-dependent protein kinase activity and Ca2+-calmodulin-dependent protein kinase activity. Phosphorylation of phospholamban at multiple sites is responsible for the various mobility forms of the holoprotein detected in SDS-polyacrylamide gels.\n" ], "offsets": [ [ 0, 2513 ] ] } ]
[ { "id": "PMID-6229539_T1", "type": "Cellular_component", "text": [ "cardiac sarcoplasmic reticulum vesicles" ], "offsets": [ [ 259, 298 ] ], "normalized": [] } ]
[]
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[]
PMID-765945
PMID-765945
[ { "id": "PMID-765945__text", "type": "abstract", "text": [ "Central nervous system infection with Eikenella corrodens: report of two cases.\nTwo cases of central nervous system infections from which E. corrodens has been isolated are reported. The portals of entry, clinical course, and antimicrobial responses conform to other reports in the literature. The importance of obtaining careful anaerobic cultures is emphasized.\n" ], "offsets": [ [ 0, 364 ] ] } ]
[ { "id": "PMID-765945_T1", "type": "Anatomical_system", "text": [ "Central nervous system" ], "offsets": [ [ 0, 22 ] ], "normalized": [] }, { "id": "PMID-765945_T2", "type": "Anatomical_system", "text": [ "central nervous system" ], "offsets": [ [ 93, 115 ] ], "normalized": [] } ]
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PMC-2908855-caption-01
PMC-2908855-caption-01
[ { "id": "PMC-2908855-caption-01__text", "type": "caption", "text": [ "The pedigree of a Korean family with macular dystrophy demonstrating the characteristics of an autosomal dominant inheritance trait.\n" ], "offsets": [ [ 0, 133 ] ] } ]
[ { "id": "PMC-2908855-caption-01_T1", "type": "Tissue", "text": [ "macular" ], "offsets": [ [ 37, 44 ] ], "normalized": [] } ]
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PMID-20460116
PMID-20460116
[ { "id": "PMID-20460116__text", "type": "abstract", "text": [ "Pain assessment by continuous EEG: association between subjective perception of tonic pain and peak frequency of alpha oscillations during stimulation and at rest.\nRecordings of neurophysiological brain responses to noxious stimuli have been traditionally based on short stimuli, in the order of milliseconds, which induce distinct event-related potentials (ERPs). However, using such stimuli in the experimental setting is disadvantageous as they are too brief to faithfully simulate clinical pain. We aimed at utilizing continuous EEG to investigate the properties of peak alpha frequency (PAF) as an objective cortical measure associated with subjective perception of tonic pain. Five minute long continuous EEG was recorded in 18 healthy volunteers under: (i) resting-state; (ii) innocuous temperature; and (iii) psychophysically-anchored noxious temperature. Numerical pain scores (NPSs) collected during the application of tonic noxious stimuli were tested for correlation with peak frequencies of alpha power-curves derived from central, temporal and frontal electrodes. NPSs and PAFs remained stable throughout the recording conditions (RM-ANOVAs; Ps>0.51). In the noxious condition, PAFs obtained at the bilateral temporal scalp were correlated with NPSs (Ps<0.001). Moreover, resting-state PAFs recorded at the bilateral temporal scalp were correlated with NPSs reported during the noxious condition (Ps<0.01). These psychophysical-neurophysiological relations attest to the properties of PAF as a novel cortical objective measure of subjective perception of tonic pain. Moreover, resting-state PAFs might hold inherent pain modulation attributes, possibly enabling the prediction of individual responsiveness to prolonged pain. The relevance of PAF to the neural processing of tonic pain may indicate its potential to advance pain research as well as clinical pain characterization.\n" ], "offsets": [ [ 0, 1894 ] ] } ]
[ { "id": "PMID-20460116_T1", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 197, 202 ] ], "normalized": [] }, { "id": "PMID-20460116_T2", "type": "Multi-tissue_structure", "text": [ "cortical" ], "offsets": [ [ 613, 621 ] ], "normalized": [] }, { "id": "PMID-20460116_T3", "type": "Multi-tissue_structure", "text": [ "cortical" ], "offsets": [ [ 1514, 1522 ] ], "normalized": [] }, { "id": "PMID-20460116_T4", "type": "Cell", "text": [ "neural" ], "offsets": [ [ 1767, 1773 ] ], "normalized": [] }, { "id": "PMID-20460116_T5", "type": "Multi-tissue_structure", "text": [ "temporal scalp" ], "offsets": [ [ 1223, 1237 ] ], "normalized": [] }, { "id": "PMID-20460116_T6", "type": "Multi-tissue_structure", "text": [ "temporal scalp" ], "offsets": [ [ 1331, 1345 ] ], "normalized": [] } ]
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PMC-2959025-sec-14
PMC-2959025-sec-14
[ { "id": "PMC-2959025-sec-14__text", "type": "sec", "text": [ "Histology of the lung\nThe left lung was fixed by gentle infusion of fixative (4% paraformaldehyde) through the tracheal cannula [24]. After excision, the lung was immersed in a fresh fixative for 2 h. The lung lobe was embedded in paraffin and cut into 3 mum transverse sections, followed by immunohistochemical and chemical staining. Photomicrographs were captured using KS400 image analyze platform (Zeiss, Oberkochen, Germany) and analyzed quantitatively.\n" ], "offsets": [ [ 0, 459 ] ] } ]
[ { "id": "PMC-2959025-sec-14_T1", "type": "Organ", "text": [ "lung" ], "offsets": [ [ 17, 21 ] ], "normalized": [] }, { "id": "PMC-2959025-sec-14_T2", "type": "Organ", "text": [ "lung" ], "offsets": [ [ 31, 35 ] ], "normalized": [] }, { "id": "PMC-2959025-sec-14_T3", "type": "Multi-tissue_structure", "text": [ "tracheal" ], "offsets": [ [ 111, 119 ] ], "normalized": [] }, { "id": "PMC-2959025-sec-14_T4", "type": "Organ", "text": [ "lung" ], "offsets": [ [ 154, 158 ] ], "normalized": [] }, { "id": "PMC-2959025-sec-14_T5", "type": "Multi-tissue_structure", "text": [ "lung lobe" ], "offsets": [ [ 205, 214 ] ], "normalized": [] } ]
[]
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[]
PMID-911696
PMID-911696
[ { "id": "PMID-911696__text", "type": "abstract", "text": [ "Some findings concerning beliefs about alcoholism.\nThe beliefs that alcoholics hold about alcoholism and themselves, and the beliefs that hospital staff and other personnel hold about alcoholism, were investigated using methods derived from the repertory grid, with anonymous facial photographs as elements. Data are presented as to the degree of association of various characteristics with alcoholism for the various groups. Differences between groups, and overall changes during group psychotherapy for patients were small. The relative contribution of personal and shared aspects of belief was measured. It was found that the agreement between groups was high and closely similar to that predictable from consistencies within groups. It is concluded that there may be a very general stereotype of alcoholism, consistent with a personality disorder concept which is implicitly held even in the face of nominal acceptance of other concepts. The self constructs of alcoholics were found to be complex. In a small follow-up study of patients, there was found to be a relationship of poor outcome with tightness of construing for key constructs after psychotherapy. The implications of the findings are discussed briefly.\n" ], "offsets": [ [ 0, 1220 ] ] } ]
[ { "id": "PMID-911696_T1", "type": "Organism_subdivision", "text": [ "facial" ], "offsets": [ [ 276, 282 ] ], "normalized": [] } ]
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[]
PMID-6776697
PMID-6776697
[ { "id": "PMID-6776697__text", "type": "abstract", "text": [ "[In vitro studies of the thyroid gland regulation principles and their evaluation].\nThe free fractions of the thyroid hormone further the metabolism of the body cells and regulate the synthesis of the thyroid hormone. Once the level of FT3 and FT4 decreases. With the help of a liberation of the hormone stimulating the thyroid gland from the anterior lobe of the pituitary gland the lack of thyroid hormone is corrected. The synthesis and secretion of the thyroid gland stimulating hormone is induced by the thyreotropin releasing hormone which is given by the hypothalamus. Moreover, the organism is able as needed to carry out the monodiodation of LT4 to biologically active LT3 or biologically inactive so-called revers T3 (RT3). The estimation of thyroid gland stimulating hormone before and 30 minutes after intravenous application of thyreotropin releasing hormone has its main importance for the early recognition of a disturbance of the regulating circle hypophysis-thyroid gland, above all in the diagnosis of clinically not yet manifest clinical pictures, such as the latent hypothyreosis and the latent hyperthyreosis, respectively (Basedow hyperthyreosis and thyroidal autonomy). According to the questioning the estimations of the levels of the thyroid hormones and of the thyroid gland stimulating hormone should be used stepwise.\n" ], "offsets": [ [ 0, 1346 ] ] } ]
[ { "id": "PMID-6776697_T1", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 25, 38 ] ], "normalized": [] }, { "id": "PMID-6776697_T3", "type": "Cell", "text": [ "body cells" ], "offsets": [ [ 156, 166 ] ], "normalized": [] }, { "id": "PMID-6776697_T5", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 320, 333 ] ], "normalized": [] }, { "id": "PMID-6776697_T6", "type": "Multi-tissue_structure", "text": [ "anterior lobe" ], "offsets": [ [ 343, 356 ] ], "normalized": [] }, { "id": "PMID-6776697_T7", "type": "Organ", "text": [ "pituitary gland" ], "offsets": [ [ 364, 379 ] ], "normalized": [] }, { "id": "PMID-6776697_T9", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 457, 470 ] ], "normalized": [] }, { "id": "PMID-6776697_T10", "type": "Multi-tissue_structure", "text": [ "hypothalamus" ], "offsets": [ [ 562, 574 ] ], "normalized": [] }, { "id": "PMID-6776697_T11", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 752, 765 ] ], "normalized": [] }, { "id": "PMID-6776697_T12", "type": "Multi-tissue_structure", "text": [ "intravenous" ], "offsets": [ [ 814, 825 ] ], "normalized": [] }, { "id": "PMID-6776697_T13", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 975, 988 ] ], "normalized": [] }, { "id": "PMID-6776697_T15", "type": "Organ", "text": [ "thyroid gland" ], "offsets": [ [ 1287, 1300 ] ], "normalized": [] } ]
[]
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[]
PMID-20433031
PMID-20433031
[ { "id": "PMID-20433031__text", "type": "abstract", "text": [ "Is the elimination of HIV infection within reach in the United States? Lessons from an epidemiologic transmission model.\nRecent estimates show that the transmission rate of human immunodeficiency virus (HIV) in the U.S. has substantially decreased. This raises the question, is elimination of HIV infection in the nation feasible in the foreseeable future? We demonstrate that if the HIV transmission rate were reduced by 50%, then the reproductive rate of HIV infection would drop below unity and lead to eventual elimination of infection. In recent congressional testimony, the director of the Centers for Disease Control and Prevention and others asserted that the HIV transmission rate can be halved by 2020, if not earlier, provided sufficient investment is made toward achieving this goal. We assert that if adequate investment is made and the transmission rate is in fact lowered by 50%, then the HIV reproductive rate would fall below unity, setting the stage for eventual elimination of HIV infection in the U.S.\n" ], "offsets": [ [ 0, 1022 ] ] } ]
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PMID-9503276
PMID-9503276
[ { "id": "PMID-9503276__text", "type": "abstract", "text": [ "Clozapine-induced agranulocytosis and thrombopenia in a patient with dopaminergic psychosis.\nIn patients with Parkinson' disease and dopaminergic psychosis, clozapine treatment is recommended as the drug is free from extrapyramidal side effects and does not worsen motor symptoms of the underlying disease. The use of clozapine, however, is limited due to its hematotoxic side effects. For treatment of clozapine-induced agranulocytosis, granulocyte colony-stimulating factors (G-CSF) are recommended. We report the case of a 72-years-old male patient with clozapine-induced agranulocytosis and thrombopenia. Neutropenia was successfully treated with G-CSF, but thrombopenia persisted and resolved spontaneously after 14 days. Bone marrow toxicity of clozapine is not restricted to white cell maturation, but may also impair thrombocytopoesis.\n" ], "offsets": [ [ 0, 844 ] ] } ]
[ { "id": "PMID-9503276_T1", "type": "Multi-tissue_structure", "text": [ "Bone marrow" ], "offsets": [ [ 727, 738 ] ], "normalized": [] }, { "id": "PMID-9503276_T2", "type": "Cell", "text": [ "white cell" ], "offsets": [ [ 782, 792 ] ], "normalized": [] } ]
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PMID-7969665
PMID-7969665
[ { "id": "PMID-7969665__text", "type": "abstract", "text": [ "Appetite regulation by serotoninergic mechanisms and effects of d-fenfluramine.\nIn this literature review, evidence is presented for the theory that the neurotransmitter, serotonin (5-hydroxytryptamine, 5HT), in medial hypothalamic centres is an important regulator for appetite and for the selection of major food constituents. High local levels of 5HT cause a reduction of appetite and a preference for protein, low levels the opposite. The main antagonistic system is noradrenergic. The drug d-fenfluramine mimics the effects of 5HT by releasing 5HT from serotoninergic nerve endings and inhibiting its neuronal re-uptake. Further experimental data prove that a high-carbohydrate, low-protein diet promotes uptake of serum tryptophan in the brain and its conversion into 5HT. Hence, this serotoninergic system may function as a self-regulatory mechanism. In patients with decreased peripheral insulin sensitivity, the system may be disturbed, causing overconsumption of carbohydrates. This is sometimes compulsive (\"carbohydrate craving\"). It may be presumed that in the treatment of obesity, in addition to the use of serotoninergic drugs, successes with reducing diets may be enhanced by including periods of high-carbohydrate, low-protein intake. It would be worthwhile to explore whether similar alimentary self-regulatory mechanisms of neurotransmitter function exist in other regulatory systems.\n" ], "offsets": [ [ 0, 1405 ] ] } ]
[ { "id": "PMID-7969665_T1", "type": "Multi-tissue_structure", "text": [ "medial hypothalamic centres" ], "offsets": [ [ 212, 239 ] ], "normalized": [] }, { "id": "PMID-7969665_T2", "type": "Multi-tissue_structure", "text": [ "nerve" ], "offsets": [ [ 573, 578 ] ], "normalized": [] }, { "id": "PMID-7969665_T3", "type": "Cell", "text": [ "neuronal" ], "offsets": [ [ 606, 614 ] ], "normalized": [] }, { "id": "PMID-7969665_T4", "type": "Organism_substance", "text": [ "serum" ], "offsets": [ [ 720, 725 ] ], "normalized": [] }, { "id": "PMID-7969665_T5", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 744, 749 ] ], "normalized": [] } ]
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PMID-21913457
PMID-21913457
[ { "id": "PMID-21913457__text", "type": "abstract", "text": [ "[Rubella in Poland in 2009].\nIn Poland, 7,587 cases of rubella were registered in 2009 (incidence 19.9 per 100,000 population). According to a new rubella case definition, introduced in 2009, 7 (0.1%) cases were classified as confirmed cases, 30 (0.4%) as probable. One case of congenital rubella syndrome was reported. The incidence in men (26.6) was 1.9-times higher than in women (13.6). The highest incidence was observed in children aged 7 and 8 years (180.3 and 175.6, respectively). No rubella deaths were registered. An improvement of laboratory diagnosis of reported cases is necessary to assess the impact of 2-dose immunization implemented in 2003 on rubella epidemiology in Poland.\n" ], "offsets": [ [ 0, 694 ] ] } ]
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PMC-2774332-sec-09
PMC-2774332-sec-09
[ { "id": "PMC-2774332-sec-09__text", "type": "sec", "text": [ "Target volumes' coverage\nThe mean PTV1 and PTV2 volumes were 452 cm3 (range 276-1074 cm3) and 300 cm3 (range 137-567 cm3) respectively. A mean of >98% (range 92-100%) of the PTV1 received 100% of the prescribed dose in all planning methods. A mean of 95.5% and 95.7% of the PTV2 received 100% of the prescribed dose with TOMO and IMRT plans respectively. A mean of 94% and 92% of the PTV2 received 100% of the prescribed dose with IB and 3D treatment plans, respectively. The mean IB and 3D plans PTV2 coverage was significantly inferior then the IMRT and TOMO plans (p < 0.02, for all comparisons).\nThe mean Inhomogeneity Coefficient (IC) was significantly lower (better) with the TOMO plans, compared to all other plans for both PTV1 and PTV2 (p < 0.0003 for all comparisons) (figure 3). The mean IC of the IMRT plans was significantly higher (worse) than the mean IC of the 3D plans regarding PTV 1 (p < 0.02) and higher (worse) then the mean IC of the IB plans regarding PTV2 (p < 0.03) (figure 3). No significant difference was found between the means of the IC of the 3D and IB plans.\nFigure 3\nThe mean Inhomogeneity Coefficient (IC) achieved by the different planning methods. The mean of the Inhomogeneity Coefficient is a measure of dose inhomogeneity in the target volumes. The closer the IC to zero, the more homogenous the dose is.\n" ], "offsets": [ [ 0, 1344 ] ] } ]
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PMC-3112138-sec-20
PMC-3112138-sec-20
[ { "id": "PMC-3112138-sec-20__text", "type": "sec", "text": [ "Acknowledgements\nThe authors gratefully acknowledge the support of DRUID study participants, study staff, members of the Indigenous Steering Group, and partner organisations. The DRUID Study was funded by the National Health and Medical Research Council (NHMRC Project Grant #236207), with additional support from the Australian Government Department of Employment and Workplace Relations, the Clive and Vera Ramaciotti Foundation, the Vincent Fairfax Family Foundation, the International Diabetes Institute (AusDiab Partnership), and Bayer HealthCare. The DRUID Study is an in-kind project of the Cooperative Research Centre for Aboriginal Health. LMB had a NHMRC Scholarship 2003-5 and is supported by NHMRC Training Fellowship (#605837), NHMRC #320860 and the Centre of Clinical Research Excellence in Clinical Science in Diabetes, University of Melbourne. JC was supported by a NHMRC Career Development Award (#283310) and a NHMRC Research Fellowship (#545200). AH is supported by NHMRC Fellowship (#520316). Thank you to Dr Jaquelyne Hughes for comments on the manuscript. Funding sources played no role in the study design, in the collection, analysis and interpretation of the data, in the writing of the manuscript, or in the decision to submit the manuscript for publication.\n" ], "offsets": [ [ 0, 1285 ] ] } ]
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PMC-2998423-sec-17
PMC-2998423-sec-17
[ { "id": "PMC-2998423-sec-17__text", "type": "sec", "text": [ "Real time RT-PCR\nRNA extraction and real-time RT-PCR were performed as we described previously [22]. The sequences of ABCG2 primers are 5'-GGCTTTCTACCTGCACGAAAACCAGTTGAG-3' (forward) and 5'-ATGGCGTTGAGACCAG-3' (reverse). The sequences of GAPDH primers are 5'-AAGGACTCATGACCACAGTCCAT-3' (forward) and 5'-CCATCACGCCACAGTTTCC-3' (reverse). The relative ABCG2 RNA level (2DeltaCT) treated with inhibitors was expressed as percentage of the control (in the presence of 0.1% DMSO) where DeltaCT (threshold cycle) = (CTABCG2-CTGAPDH).\n" ], "offsets": [ [ 0, 528 ] ] } ]
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PMC-1896192-sec-09
PMC-1896192-sec-09
[ { "id": "PMC-1896192-sec-09__text", "type": "sec", "text": [ "Supporting Information\nAlternate Language Article S1\nTranslation of the manuscript into French by EL\n(201 KB DOC).\nClick here for additional data file.\n" ], "offsets": [ [ 0, 152 ] ] } ]
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PMID-16201626
PMID-16201626
[ { "id": "PMID-16201626__text", "type": "abstract", "text": [ "Polybrominated diphenyl ethers in indoor dust in Ottawa, Canada: implications for sources and exposure.\nPolybrominated diphenyl ethers (PBDEs) are widely used as additive flame retardants in plastics, soft furnishings, electrical and electronic equipment, and insulation in the indoor environment, and may be released indoors via volatilization or as dusts. The penta-and octa-brominated mixes are now banned in most parts of Europe, and phasing out of their use has recently begun in North America. This study follows a previous investigation into indoor air levels of PBDEs. House dust was analyzed from the family vacuum cleaners of 68 of the same 74 randomly selected homes, in Ottawa, Canada during the winter of 2002-2003. PBDEs, comprising on average 42% BDE-209, were found in all samples. The levels were log-normally distributed with a geometric mean sigmaPBDE of 2000 ng g(-1), and a median of 1800 ng g(-1) dust. The levels in dust did not correlate with questionnaire information on house characteristics. Correlations were found between pentamix congener levels in dust and in air from the same homes, but not for congeners of the more highly brominated mixes. Exposure scenarios are presented for mean and high dust ingestion rates, and compared against exposures from other pathways, for both adults and toddlers (6 months-2 years). Assuming a mean dust ingestion rate and median dust and air concentrations, adults would be exposed to ca. 7.5 ng sigmaPBDE d(-1) via the dust ingestion pathway, which represents approximately 14% of total daily exposure when compared to diet (82%) and inhalation (4%). However, for toddlers the equivalent intakes would be 99 ng d(-1), representing 80% of their daily PBDE exposure. At high dust ingestion rates these values increase to 180 ng d(-1) (80% daily intake) for adults and 360 ng d(-1) (89% daily intake) for toddlers. The data give a clearer picture of sources of PBDE exposure in the home environment and suggest that dust could be a significant exposure pathway for some individuals, particularly children.\n" ], "offsets": [ [ 0, 2071 ] ] } ]
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PMID-9421512
PMID-9421512
[ { "id": "PMID-9421512__text", "type": "abstract", "text": [ "Effect of a mutation in the anticodon of human mitochondrial tRNAPro on its post-transcriptional modification pattern.\nAlthough the gene sequences of all 22 tRNAs encoded in the human mitochondrial genome are known, little information exists about their sequences at the RNA level. This becomes a crucial limitation when searching for a molecular understanding of the growing number of maternally inherited human diseases correlated with point mutations in tRNA genes. Here we describe the sequence of human mt-tRNAPropurified from placenta. It shows absence of editing events in this tRNA and highlights the presence of eight post-transcriptional modifications. These include T54, never found so far in an animal mt-tRNA, and m1G37, a modification known to have fundamental functional properties in a number of canonical tRNAs. Occurrence of m1G37 was further investigated in an analysis of the substrate properties of in vitro transcripts of human mt-tRNAProtowards pure Escherichia coli methylguanosine transferase. This enzyme properly methylates G37 in mt-tRNA and is sensitive to the presence of a second G at position 36, neighboring the target nucleotide for methylation. Since mutation of nt 36 was shown to be correlated with myopathy, the potential consequences of non-modification or under-modification of mt-tRNA nucleotides in expression of the particular myopathy and of mitochondrial diseases in general are discussed.\n" ], "offsets": [ [ 0, 1435 ] ] } ]
[ { "id": "PMID-9421512_T1", "type": "Cellular_component", "text": [ "mitochondrial" ], "offsets": [ [ 47, 60 ] ], "normalized": [] }, { "id": "PMID-9421512_T2", "type": "Cellular_component", "text": [ "mitochondrial genome" ], "offsets": [ [ 184, 204 ] ], "normalized": [] }, { "id": "PMID-9421512_T3", "type": "Organ", "text": [ "placenta" ], "offsets": [ [ 532, 540 ] ], "normalized": [] }, { "id": "PMID-9421512_T4", "type": "Cellular_component", "text": [ "mitochondrial" ], "offsets": [ [ 1386, 1399 ] ], "normalized": [] } ]
[]
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PMID-8643685
PMID-8643685
[ { "id": "PMID-8643685__text", "type": "abstract", "text": [ "Human immunodeficiency virus type 1 viral background plays a major role in development of resistance to protease inhibitors.\nThe observed in vitro and in vivo benefit of combination treatment with anti-human immunodeficiency virus (HIV) agents prompted us to examine the potential of resistance development when two protease inhibitors are used concurrently. Recombinant HIV-1 (NL4-3) proteases containing combined resistance mutations associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme activity. Subsequent construction of HIV-1 (NL4-3) proviral clones containing the same mutations yielded viruses that were severely impaired in growth or nonviable, confirming that combination therapy may be advantageous. However, passage of BMS-186318-resistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug treatment, produced viable viruses resistant to both BMS-186318 and the second compound. The predominant breakthrough virus contained the G48V/A71T/V82A protease mutations. The clone-purified RF (G48V/A71T/V82A) virus, unlike the corresponding defective NL4-3 triple mutant, grew well and displayed cross-resistance to four distinct protease inhibitors. Chimeric virus and in vitro mutagenesis studies indicated that the RF-specific protease sequence, specifically the Ile at residue 10, enabled the NL4-3 strain with the triple mutant to grow. Our results clearly indicate that viral genetic background will play a key role in determining whether cross-resistance variants will arise.\n" ], "offsets": [ [ 0, 1578 ] ] } ]
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PMC-3082541-caption-03
PMC-3082541-caption-03
[ { "id": "PMC-3082541-caption-03__text", "type": "caption", "text": [ "Loss of body weight after challenge-infection with WNV.\nMice (n = 8) were vaccinated intranasally with Flu-NA-DIII (*) or Flu-NA-GFP (o) or by the subcutaneous route (^ and ^, respectively). The daily weights of each animal were calculated compared to their respective weight on the day of challenge, and data are shown as the average percentage of initial weight for each group. Error bars represent the standard error for all samples available at that time point. Subsequently, the mice were challenged subcutaneously with 106 TCID50 WNV-NY99 and weighed daily. The mean body weight is expressed as the percentage of the body weight before challenge infection (A). The survival rates of mice after challenge infection with WNV-NY99 are depicted as Kaplan-Meier survival curves (B). The difference in survival rate between Flu-NA-DIII and Flu-NA-GFP vaccinated mice was statistically significant as determined by the logrank test. The symbols for the respective groups are the same as in panel A.\n" ], "offsets": [ [ 0, 998 ] ] } ]
[ { "id": "PMC-3082541-caption-03_T1", "type": "Immaterial_anatomical_entity", "text": [ "intranasally" ], "offsets": [ [ 85, 97 ] ], "normalized": [] }, { "id": "PMC-3082541-caption-03_T2", "type": "Organism_subdivision", "text": [ "body" ], "offsets": [ [ 8, 12 ] ], "normalized": [] }, { "id": "PMC-3082541-caption-03_T3", "type": "Organism_subdivision", "text": [ "body" ], "offsets": [ [ 573, 577 ] ], "normalized": [] }, { "id": "PMC-3082541-caption-03_T4", "type": "Organism_subdivision", "text": [ "body" ], "offsets": [ [ 623, 627 ] ], "normalized": [] } ]
[]
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PMC-3199853-sec-07
PMC-3199853-sec-07
[ { "id": "PMC-3199853-sec-07__text", "type": "sec", "text": [ "Patients and Study Design\nA prospective evaluation of the different CMR parameters for predicting LV segmental and global functional recovery was performed in 46 patients (63 +/- 10 years old, 3 with previous CABG, 35 with three-vessel disease, 3 with one-vessel disease) with LV systolic dysfunction (LVEF 35 +/- 8%) before they underwent surgical (n = 34) or percutaneous (n = 12) revascularisation. Sixty patients without contraindications for CMR were screened for the following inclusion criteria: (1) CAD (> 70% stenosis in one or more major epicardial vessels), scheduled for a revascularisation procedure; (2) LVEF <= 45%; (3) at least two adjacent segments with wall motion abnormalities at rest; and (4) no infarction or revascularisation within the last two months. Patients were included in the study only after a successful and complete coronary revascularisation. Of the 14 patients who did not complete the study, 3 decided not to undergo the repeated CMR scan or were lost during follow-up; 7 had significant periprocedural injury (new LGE zones on repeated CMR scans and clinically proven periprocedural myocardial infarction (MI) or MI between both scans); 3 had pacemakers or defibrillators implanted in the period between the MR scans; and 1 was excluded because of dilated cardiomyopathy with secondary CAD. None of the patients were excluded from the study for technical reasons or image quality.\nThe mean interval between CMR and revascularisation was 12 +/- 13 days, and none of the patients presented clinical evidence of infarction during this period. The mean interval between MI and the first CMR was 3.6 years. In 46 patients, the extent of regional contractility and LGE were determined repeatedly by CMR 28 +/- 4 weeks (6 months) after revascularisation.\nThe study was approved by the Lithuanian Bioethics Committee (Nr. 17), and informed written consent was obtained from each patient prior to inclusion in the study.\n" ], "offsets": [ [ 0, 1950 ] ] } ]
[ { "id": "PMC-3199853-sec-07_T1", "type": "Multi-tissue_structure", "text": [ "epicardial vessels" ], "offsets": [ [ 548, 566 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T2", "type": "Multi-tissue_structure", "text": [ "coronary" ], "offsets": [ [ 850, 858 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T3", "type": "Multi-tissue_structure", "text": [ "myocardial" ], "offsets": [ [ 1121, 1131 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T4", "type": "Pathological_formation", "text": [ "LGE" ], "offsets": [ [ 1052, 1055 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T5", "type": "Pathological_formation", "text": [ "LGE" ], "offsets": [ [ 1697, 1700 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T6", "type": "Multi-tissue_structure", "text": [ "wall" ], "offsets": [ [ 671, 675 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T7", "type": "Multi-tissue_structure", "text": [ "LV" ], "offsets": [ [ 98, 100 ] ], "normalized": [] }, { "id": "PMC-3199853-sec-07_T8", "type": "Multi-tissue_structure", "text": [ "LV" ], "offsets": [ [ 277, 279 ] ], "normalized": [] } ]
[]
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[]
PMC-3159351-sec-02
PMC-3159351-sec-02
[ { "id": "PMC-3159351-sec-02__text", "type": "sec", "text": [ "Materials and Methods:\nA total of 75 brain abscess pus specimens were collected during neurosurgery, either by burr hole or by craniotomy. These specimens were further subjected to Gram stain, Ziehl-Neelsen (ZN) stain, and conventional microbiological culture. Only those cases which showed presence of AFB on ZN stain along with the growth of Mycobacterium tuberculosis were considered as TBAs. Such TBA cases were further presented along with their In vitro Proton Magnetic Resonance (MR) Spectroscopic findings.\n" ], "offsets": [ [ 0, 515 ] ] } ]
[ { "id": "PMC-3159351-sec-02_T1", "type": "Multi-tissue_structure", "text": [ "brain abscess pus specimens" ], "offsets": [ [ 37, 64 ] ], "normalized": [] }, { "id": "PMC-3159351-sec-02_T2", "type": "Multi-tissue_structure", "text": [ "specimens" ], "offsets": [ [ 145, 154 ] ], "normalized": [] } ]
[]
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PMC-2822164-caption-01
PMC-2822164-caption-01
[ { "id": "PMC-2822164-caption-01__text", "type": "caption", "text": [ "Demographic data of subjects\n" ], "offsets": [ [ 0, 29 ] ] } ]
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[]
[]
[]
PMC-3039624-sec-11
PMC-3039624-sec-11
[ { "id": "PMC-3039624-sec-11__text", "type": "sec", "text": [ "The importance in identifying genes involved in spinal curvature\nSpinal curvature is a prevalent and costly deformity among humans and teleosts. The estimated annual cost of treating children hospitalized with idiopathic scoliosis (IS) in the United States alone is over $3 billion. This cost estimate does not consider Scheuermann kyphosis, or adults with idiopathic-type spinal curvature who suffer from chronic back pain, contributing to the estimated $849 billion cost of treatment and lost wages associated with musculoskeletal disease [24]. Among teleosts, spinal column deformities reduce total production in the aquaculture industry substantially [12]. In contrast to humans, teleost curve phenotypes are less well characterized; although heritable curves are acknowledged to account for many cases among cultured stocks, whether these cases are from congenital defects or are idiopathic-type is often not known.\nDespite the prevalence and impact of this type of deformity, the genetic architecture and specific genes involved are unknown. The current view is that human idiopathic-type scoliosis is a complex genetic disorder with multiple genes segregating in the population exhibiting complex genotype by environment interactions [25-30]. In aquaculture stocks, inheritance for spinal curvature has been described as Mendelian recessive or dominant, as well as polygenic, depending on how well the phenotype is characterized and what stock is considered (reviewed in [13], [16]). The guppy curveback phenotype has been extensively characterized so that the lineage can be applied as a model for understanding the biological context of heritable spinal curvature [1,7-9]. Future studies can use approaches to map QTL affecting shape based on digital photos [31,32], rather than the qualitative scale used in the present study. The identification of QTL in this study is a first step in understanding the genetics of this type of deformity and will lead to the identification of biological pathways associated with spinal integrity.\n" ], "offsets": [ [ 0, 2042 ] ] } ]
[ { "id": "PMC-3039624-sec-11_T1", "type": "Organism_subdivision", "text": [ "spinal" ], "offsets": [ [ 48, 54 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T2", "type": "Organism_subdivision", "text": [ "Spinal" ], "offsets": [ [ 65, 71 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T3", "type": "Organism_subdivision", "text": [ "back" ], "offsets": [ [ 414, 418 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T4", "type": "Organism_subdivision", "text": [ "spinal" ], "offsets": [ [ 373, 379 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T5", "type": "Anatomical_system", "text": [ "musculoskeletal" ], "offsets": [ [ 517, 532 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T6", "type": "Organism_subdivision", "text": [ "spinal column" ], "offsets": [ [ 563, 576 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T7", "type": "Organism_subdivision", "text": [ "spinal" ], "offsets": [ [ 1289, 1295 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T8", "type": "Organism_subdivision", "text": [ "spinal" ], "offsets": [ [ 1656, 1662 ] ], "normalized": [] }, { "id": "PMC-3039624-sec-11_T9", "type": "Organism_subdivision", "text": [ "spinal" ], "offsets": [ [ 2024, 2030 ] ], "normalized": [] } ]
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PMID-14663884
PMID-14663884
[ { "id": "PMID-14663884__text", "type": "abstract", "text": [ "[Laboratory diagnostics of Crimean hemorrhagic fever by polymerase chain reaction].\nOur group developed, within the present case study, two techniques' variations, i.e. a single-step RT-PCR and nested RT-PCR assays, for the purpose of detecting the Crimean-Congo hemorrhagic fever RNA virus in human samples. The above assays as well as those previously recommended by the Ministry of Health of the Russian Federation were simultaneously used in 14 clinical samples obtained from patients with Crimean hemorrhagic fever. After assessing the detection accuracy, it was found that the developed-by-us test system displayed the same or even better diagnostic values versus the previously recommended nested RT-PCR and a 1000-fold advantage over the previously recommended single-step RT-PCA. The single-step RT-PCR assay variation is always more preferable in sense of technical and economic motivations. Finally, the test system developed by us has every reason to become the method of choice in routine PCR diagnosis of Crimean hemorrhagic fever after all official trials and approvals are duly complied with.\n" ], "offsets": [ [ 0, 1109 ] ] } ]
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PMID-21822531
PMID-21822531
[ { "id": "PMID-21822531__text", "type": "abstract", "text": [ "Massive osteolysis in a dog resembling Gorham's disease in humans.\nAn eight-month-old mixed-breed dog was presented with a history of sudden onset pelvic limb lameness. Radiographic and computed tomographic examinations demonstrated an osteolytic process involving the lumbar spine and pelvis. A comprehensive work-up including serial radiographic skeletal survey, biopsy, routine laboratory investigation and evaluation of parathyroid hormone (PTH) and 25-hydroxy-vitamin D levels failed to reveal any underlying cause for the osteolysis. Conservative treatment using the bisphosphonate drug alendronate and oral analgesic medications resulted in a return to nearly normal long-term function, despite massive lumbar and pelvic osteolysis. The clinical, radiological and histopathological features in this dog are reported, and similarities with the human condition known as Gorham's disease are discussed.\n" ], "offsets": [ [ 0, 907 ] ] } ]
[ { "id": "PMID-21822531_T1", "type": "Organism_subdivision", "text": [ "pelvic limb" ], "offsets": [ [ 147, 158 ] ], "normalized": [] }, { "id": "PMID-21822531_T2", "type": "Organ", "text": [ "lumbar spine" ], "offsets": [ [ 269, 281 ] ], "normalized": [] }, { "id": "PMID-21822531_T3", "type": "Organ", "text": [ "pelvis" ], "offsets": [ [ 286, 292 ] ], "normalized": [] }, { "id": "PMID-21822531_T4", "type": "Anatomical_system", "text": [ "skeletal" ], "offsets": [ [ 348, 356 ] ], "normalized": [] } ]
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PMC-2677866-sec-12
PMC-2677866-sec-12
[ { "id": "PMC-2677866-sec-12__text", "type": "sec", "text": [ "Nucleotide features of free-standing homing-endonucleases\nGene control elements were identified for several members of each type of intervening homing endonuclease genes described in this study. In 15 out of 16, 5' untranslated regions of the endonucleases we identified RNA hairpin structures upstream of initiation codons (Figures 1 and 4A). This may be a translational regulatory hairpin structure known from various phage genes, including homing endonucleases (22,47-49). The hairpins we found are in fractured gene loci with different protein host types, including gp41, IMPDH, DnaE, NrdJ and NrdA. Ten of these hairpins also include a conserved sequence of Aeh1 phage late promoter element (TATAAATA), which was recently shown to inhibit the translation of a gene-fracturing endonuclease gene, by sequestering its ribosome binding site (22,23). Analysis of the endonuclease 5' untranslated regions revealed two conserved motifs (Figures 4A and Supplementary Figure S4), which usually complement each other on the stem of the conserved hairpin structures. \nFigure 4.\nNucleotide features of endonuclease genes. (A) RNA hairpin structures at the 5' untranslated region of endonuclease ORFs in the gp41-1 (representing the very similar sequences of gp41-1-7), nrdA-5 and DnaE-1 gene loci. Initiator codons are marked by arrows, conserved putative T4 late promoter elements are boxed, and conserved sequence motifs (Supplementary Figure S4) are highlighted in grey. The expected values for motifs 1 and 2 are 1.7-10 and 9.9-3, respectively. RNA structures were calculated using the Vienna package (http://rna.tbi.univie.ac.at/cgi-bin/RNAfold.cgi), and sequence motifs were identified using the MEME program. (B) Overlapping#protein coding regions of endonuclease 3' termini and the 5' termini of their downstream genes.\nAdditionally, 15 loci included an overlapping region of 6-69 bp between the coding regions of the probable endonuclease C-termini and the downstream N-termini of the split-intein part (Figures 1 and 4B). This overlap is present in both types of endonucleases, and is independent on the presence of a split-intein part in the fractured gene, also occurring in the putative sbcD DNA-repair gene that we found, as well as in the Aeh1 fractured nrdA found by Gibb and Edgell (22).\n" ], "offsets": [ [ 0, 2298 ] ] } ]
[ { "id": "PMC-2677866-sec-12_T1", "type": "Cellular_component", "text": [ "ribosome" ], "offsets": [ [ 820, 828 ] ], "normalized": [] } ]
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PMC-2721088-sec-10
PMC-2721088-sec-10
[ { "id": "PMC-2721088-sec-10__text", "type": "sec", "text": [ "Chicken CCN3 expression in embryonic and extraembryonic tissues\nExpression of CCN3 in axial structure becomes visible in the presegmentation stage and reaches to the highest level at the beginning of somitogenesis (HH stage 7, Fig. 1a). Strong similarity between CCN3 and Sonic Hedgehog was observed for the expression pattern in axial structure (notochord and floor plate), in which the left-right asymmetrical pattern in the node area is also conserved (Fig. 1b). However, Sonic Hedgehog expression is slightly broader than that of CCN3. Since CCN3 stimulates Notch signaling (Sakamoto et al. 2002), we investigated the expression of Notch signal genes. Among them, Serrate1, a ligand of Notch is unique because its expression is apparently a right deviated pattern in the node area (Fig. 1c). Another Notch ligand, Delta1 shows a right deviated pattern, but is more caudal area of the node extending to the primitive streak (data not shown). The expression of CCN3 in axial structure was followed by the presomitic mesoderm although it is diminished (Sakamoto et al. 2002). \nFig. 1\nExpression of mRNA in early stage chicken embryo; CCN3 (a), Sonic Hedgehog (b) and Serrate1 (c) at the beginning stage of somitogenesis (Hamburger and Hamilton (HH) Stage 7). Arrowheads indicate Hensen's node. Demonstrates the schematic view of tissue organization at this stage (d). Expression of CCN3 mRNA in blood islands of chicken extraembryonic tissue (HH stage 10) (e). Ventral part of the endothelial precursor cells in blood islands is positive for CCN3 expression. Coloration was stopped before the background staining started in sense probes (negative control)\nThere is accumulating evidence of CCN3 commitment to hematopoiesis and therefore we investigated the CCN3 expression in extraembryonic tissues. Blood islands are formed in the yolk sac mesodermal area just between the visceral endodermal and ectodermal layers, which supply the red blood cells at the primary stage. The cells in blood islands are called hemangioblasts since they also differentiate into the endothelial cells of extraembryonic blood vessel structure. In chicken embryo, differentiating endothelial cells in the ventral part of blood islands express CCN3 from the initial stage (Fig. 1e). Erythroblasts in the center of blood islands (spherical cells in Fig. 1e) weakly express CCN3 and their expression is mildly enhanced in later stage (data not shown).\n" ], "offsets": [ [ 0, 2429 ] ] } ]
[ { "id": "PMC-2721088-sec-10_T1", "type": "Tissue", "text": [ "embryonic" ], "offsets": [ [ 27, 36 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T2", "type": "Tissue", "text": [ "extraembryonic tissues" ], "offsets": [ [ 41, 63 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T3", "type": "Developing_anatomical_structure", "text": [ "embryo" ], "offsets": [ [ 1127, 1133 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T4", "type": "Tissue", "text": [ "tissue" ], "offsets": [ [ 1330, 1336 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T6", "type": "Tissue", "text": [ "extraembryonic tissue" ], "offsets": [ [ 1421, 1442 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T7", "type": "Cell", "text": [ "endothelial precursor cells" ], "offsets": [ [ 1482, 1509 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T8", "type": "Organism_substance", "text": [ "blood islands" ], "offsets": [ [ 1396, 1409 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T5", "type": "Organism_substance", "text": [ "blood islands" ], "offsets": [ [ 1513, 1526 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T9", "type": "Tissue", "text": [ "extraembryonic tissues" ], "offsets": [ [ 1777, 1799 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T10", "type": "Organism_substance", "text": [ "Blood islands" ], "offsets": [ [ 1801, 1814 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T11", "type": "Tissue", "text": [ "yolk sac mesodermal" ], "offsets": [ [ 1833, 1852 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T12", "type": "Tissue", "text": [ "visceral endodermal" ], "offsets": [ [ 1875, 1894 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T13", "type": "Tissue", "text": [ "ectodermal layers" ], "offsets": [ [ 1899, 1916 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T14", "type": "Cell", "text": [ "red blood cells" ], "offsets": [ [ 1935, 1950 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T15", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 1977, 1982 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T16", "type": "Organism_substance", "text": [ "blood islands" ], "offsets": [ [ 1986, 1999 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T17", "type": "Cell", "text": [ "hemangioblasts" ], "offsets": [ [ 2011, 2025 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T18", "type": "Cell", "text": [ "endothelial cells" ], "offsets": [ [ 2065, 2082 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T19", "type": "Developing_anatomical_structure", "text": [ "extraembryonic blood vessel structure" ], "offsets": [ [ 2086, 2123 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T20", "type": "Developing_anatomical_structure", "text": [ "embryo" ], "offsets": [ [ 2136, 2142 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T21", "type": "Cell", "text": [ "endothelial cells" ], "offsets": [ [ 2160, 2177 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T22", "type": "Organism_substance", "text": [ "blood islands" ], "offsets": [ [ 2201, 2214 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T23", "type": "Cell", "text": [ "Erythroblasts" ], "offsets": [ [ 2262, 2275 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T24", "type": "Organism_substance", "text": [ "blood islands" ], "offsets": [ [ 2293, 2306 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T25", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 2318, 2323 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T26", "type": "Multi-tissue_structure", "text": [ "ventral" ], "offsets": [ [ 2185, 2192 ] ], "normalized": [] }, { "id": "PMC-2721088-sec-10_T27", "type": "Multi-tissue_structure", "text": [ "Ventral" ], "offsets": [ [ 1462, 1469 ] ], "normalized": [] } ]
[]
[]
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PMC-2972690-sec-19
PMC-2972690-sec-19
[ { "id": "PMC-2972690-sec-19__text", "type": "sec", "text": [ "Discussion\nOur results indicate beneficial effects of motivational incentives on cognitive performance and alleviating effects on cognitive decline. These beneficial effects were evident in healthy young and older adults and in patients with Parkinson's disease. Young adults showed improved antisaccade preparation when a reward was at stake; older adults and PD patients could utilize reward prospect to improve their impaired antisaccade preparation. Elderly participants and PD patients were not only better prepared by means of commonly used preparatory aids (i.e., more preparation time and advance information on the upcoming response) but also by means of motivational incentives. These beneficial effects of motivational incentives on cognitive action preparation in healthy and pathological aging further support views that question the notion of monotonic deterioration of cognitive function with age (Allen et al., 2001). They indicate that age-related declines can be modulated by emotion-cognition interactions.\nIn line with the predominant view that cognitive control deteriorates in aging and Parkinson's disease, and in line with previous findings on age-related changes in antisaccade control specifically (Eenshuistra et al., 2004; Chan et al., 2005; Amador et al., 2006; Abel and Douglas, 2007), the current results showed decline in antisaccade preparation in PD patients with severe motor symptoms as compared to healthy seniors. Mild-symptom patients and healthy elderly did not differ in antisaccade preparation. Healthy seniors showed declining antisaccade preparation as compared to young adults. Decline was evident on several oculomotor parameters and most pronounced on antisaccade onset latencies. In line with the notion that in general, elderly tend to prefer accuracy over speed, elderly showed no decreased antisaccade accuracy as compared to young adults. As compared to the young group, elderly and PD patients exhibited slightly, but not significantly more premature eye movements. Premature eye movements, however significantly increased in elderly and PD patients but only slightly in the young, when more specific information on the upcoming movement was available in advance. Presumably, this increase in premature eye movements reflects difficulties with the inhibition of externally guided movement and/or the suppression of strongly activated prepotent action plans. On the one hand, the choice for medicated PD patients represents a limitation of the current study as we cannot exclude differential effects of medication on behavior. On the other hand, PD patients generally take medication in their daily routine, such that the results can be generalized to clinical practice. Exploratory analysis within the PD patient group revealed that patients with more severe motoric symptoms (as indexed by their motoric subscore on the UPDRS) displayed more signs of antisaccade decline, such as longer antisaccade latencies and lower accuracy compared to mildly affected patients, who initiated saccades equally fast as healthy adults. This suggests that dopaminergic medication was not sufficient to raise the patient's antisaccadic preparation up to the level of the healthy older adults.\nOne intriguing observation was that despite the different extents of observed antisaccade performance decline in elderly and PD patients, reward prospect led to beneficial effects on antisaccade latency and accuracy in young, elderly, and PD patients alike. Young, elderly and PD patients benefited from reward prospect to the same extent, confirming that the expectancy of reward is a powerful mediator of cognitive control, even if cognitive control suffers from decline. The expectation of rewarding incentives thus seems to support older adults' and PD patients' ability to anticipate, prepare and initiate goal-directed behavior.\nThese findings imply that despite a general decline in the action preparation system as indexed by increased antisaccade latency, action preparation processes remain susceptible to the prospect of future reward. It could thus be argued that the neural representations of upcoming rewards influence neural systems concerned with action preparation and oculomotor control. Although the current behavioral results cannot exclude or confirm neural links between reward anticipation and action preparation systems in the brain, they suggest intact cross-talk among subcortical circuits that allow goal-directed action to be modified by motivational factors. The motivational neural reward anticipation signal presumably activates the reward network including the amygdala, orbitofrontal cortex, the more ventral and dorsal striatum (nucleus accumbens, putamen, and caudate), leading to an release of caudate/SNr inhibition on the executive oculomotor structure superior colliculus. This transiently decreased inhibitory force on superior colliculus may improve goal-directed oculomotor control. Thus reward anticipation might compensate for the age- and disease-related dopaminergic loss in the SNc projections to the caudate/SNr and may thus play a compensatory role in \"boosting\" the efficiency of interactions between motivational and impaired cognitive control processes.\nHowever the reward-related modulation of the oculomotor control system may not only apply to the basal ganglia part of the oculomotor network. Although speculative, it could extend to the cortical eyefields (frontal, supplementary, and parietal eyefields) and to parts of the visual cortex. Human research shows that more preparatory activation in the frontal eyefields leads to a faster antisaccade latency (Connolly et al., 2002, 2005). The compensatory effect on the antisaccade latency, therefore, could theoretically stem from a propagation of reward anticipation signal in the caudate to the frontal eyefields. Complex structural connections enable the striatum to exert a controlling influence over the cerebral cortex via a series of reentrant corticobasal ganglia circuits. Thus reward anticipation may increase the level of preparation in the intact cortical eyefields and thereby compensate for age- and disease-related subcortical decrements in the oculomotor network.\nTaken together, it seems plausible that motivational reward processes in the caudate enhance preparatory activation in subcortical as well as in cortical nodes of the oculomotor network. Several neurotransmission mechanisms may underlie the remedial effect of positive incentives on declining antisaccadic control. Given the convergence of dopamine and glutamate inputs at the spiny projection neurons in the striatum (Burns et al., 1994), an interaction between dopamine and glutamate might underlie striatal processes of reward anticipation and action preparation. However, it cannot be fully excluded that alterations in other neurotransmitter systems may also have an effect on declining oculomotor control and on remediating incentive effects. Non-dopaminergic changes such as noradrenergic, serotonergic, and cholinergic deafferentation of the cortex also occur in PD and can inflict cognitive deficits (Agid et al., 1987). Evidence from non-human primates suggests that basal ganglia dopamine acts to speed motor responding in response to rewarding cues (Niv, 2007; Niv et al., 2007). Among at least five types of DA receptors, mainly D1 and D2 receptors are expressed in caudate projection neurons (Nakamura and Hikosaka, 2006). Tendencies to speed responses to obtain large rewards have been found to be dependent on striatal D1 receptors (Dalley et al., 2005; Berridge, 2007). In contrast to this D1 modulated speeding in reward-motor tasks, evidence from saccade tasks in non-human primates suggests D2 receptor modulation of reward dependent improvements of performance (Nakamura and Hikosaka, 2006). Injections of a D1 antagonist and a D2 antagonist into the region of the caudate where saccade-related neurons are clustered while the monkey performed a reward-biased saccade task showed that D1 antagonists attenuate the reward modulation of saccade behavior whereas D2 antagonists into the same region enhanced the reward-dependent changes.\nFuture studies of Parkinson patients on versus off medication, could provide some information on the role of dopaminergic mechanisms in the remedial effects on antisaccadic performance. A recent study of reward learning in Parkinson patients on/off dopaminergic medication showed that patients adapted their behavior to maximize expected reward value dependent on their medication status (Moustafa et al., 2008). Whilst off dopaminergic medication, patients slowed their responses to avoid low expected values, but succeeded less well in speeding responses when a reward was at stake. The opposite pattern emerged when the same patients were on medication; patients showed better response speeding, and worse response slowing, to maximize expected value.\nThe current behavioral findings are in line with neuroimaging research showing intact neural representations of future reward in the aging striatum (Samanez-Larkin et al., 2007). The observation however that older adults and PD patients can use this intact neural representation of reward anticipation (a positive motivational incentive) to optimize their preparatory processes, cannot necessarily be generalized to cognitive contexts with negative motivational incentives. Samanez-Larkin et al.(2010) recently showed that older adults were not able to optimally use their intact neural reward anticipation system in risky financial decision making. Elderly made more suboptimal choices when they were to choose risky assets. The authors deemed it likely that these decrements in value-based decision making are explained by the fact that value-based decision making requires the weighting of behavioral alternatives, that may lead to either gain or loss. During anticipation of rewards older adults show similar neural responses as young adults but they show reduced neural activation during the anticipation of losses (Samanez-Larkin et al., 2007). The latter, together with the observation that older adults tend to shift their attention away from negative stimuli and attend to positive information instead (Mather and Carstensen, 2003, 2005), may have led to the underestimation of loss and therefore to more risky and suboptimal decisions.\nIn this respect, one limitation of the current task is that it built solely on reward prospect and not on the prospect of loss, such that the question of how the anticipation of loss influences action preparation was not tested. The impact of negative incentives might be an intriguing question for future research, as due to the decreased activation of the neural loss anticipation system (Samanez-Larkin et al., 2007) together with the observed differential attentional bias for negative and positive information (Mather and Carstensen, 2003), it seems likely that negative motivational incentives, i.e., the prospect of loss, might have a different impact on action preparation in older adults than in the young. Future approaches to the effect of loss anticipation on declining antisaccade control may ideally contain a sequence of experiments, starting with a separate (punishment only) approach before moving to combined reward-punishment designs. This might be necessary as previous evidence (from healthy young adults) suggests that the reward effect on oculomotor control disappears in the presence of punishment trials. The authors deemed it likely that the participants increased caution to all incentive (reward and punishment) trials (Blaukopf and DiGirolamo, 2006).\nAs of yet, age-related changes in neural reward anticipation have mainly been studied in isolation. Recently however, the interaction of neural reward processing with other cognitive functions and their underlying neural systems, such as the action control system, has gained increasing interest (Haber and Knutson, 2010). Initial evidence suggests coordinated activity between distant brain regions responsible for reward processing (Cohen et al., 2009). The current results encourage further neural network investigations on the role of coordinated brain network activity in motivated behavior. Behavioral benefits from motivation might be associated with changes in functional brain connectivity on a larger scale, e.g., between frontostriatal reward and action preparation structures.\nAnother important factor that emerges from the present and previous results, is the importance of the training of the motivational aspects of the instructions that need to be kept in working memory when performing a cognitive task. Samanez-Larkin et al. (2007) found intact neural reward anticipation processes specifically in the absence of learning (after the learning process of reward cue-reward associations was completed). Therefore it might be important for researchers doing experiments with motivation based instructions to keep in mind that, compared to young adults, elderly and PD patients are generally hampered on stimulus-response learning (Shohamy et al., 2004; Marschner et al., 2005). Reward instruction cues, as they were used in the current study require participants to form reward cue-reward associations. Impairments in the learning of associations between the cue signaling reward and the actual reward might conceal intact reward anticipation processes. When the formation of associations is weakened, it could appear as a failure to capitalize on the neural reward anticipation system, whereas it represents an indirect effect of non-available reward associations in working memory when preparing the response. Hence, one might circumvent the effect of potential learning impairments on reward anticipation processes by the training of abstract reward cues (as in the current and in Samanez-Larkin's study) or by using explicit and concrete rewards. Once the learning of reward cues is accomplished the intact reward anticipation processes might become evident.\nIn sum, the results confirmed that the preparation of goal-directed actions declined in PD patients compared to healthy seniors, and in healthy seniors compared to young adults. Due perhaps to deterioration in dopaminergic striatal circuitry, antisaccade performance is subject to decline in healthy seniors, and even more in individuals with Parkinson's disease. The prospect of future reward however provided a motivational incentive for optimizing oculomotor preparation in all groups alike. These results suggest that reward-processing networks and oculomotor-control networks in the brain are connected in such a way (presumably with the dorsal striatum as a common nexus) that reward anticipation can facilitate oculomotor control and alleviate the deficiencies experienced by healthy seniors and PD patients. Future investigations should examine whether the observed effects are specific for the current task or generalize to other tasks that show age- and PD-related cognitive decrements (e.g., in task switching) and have been related to dopaminergic denervation in the caudate (e.g., impaired verbal episodic memory, attention, and response inhibition; Rinne et al., 2000; Bruck et al., 2005). Future studies on network processes may help to localize the neural link between reward prospect and action preparation that enables alleviating effects of motivational incentives on cognitive decline.\n" ], "offsets": [ [ 0, 15437 ] ] } ]
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"text": [ "neural" ], "offsets": [ [ 4302, 4308 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T11", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 4381, 4386 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T12", "type": "Multi-tissue_structure", "text": [ "subcortical" ], "offsets": [ [ 4425, 4436 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T13", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 4535, 4541 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T14", "type": "Multi-tissue_structure", "text": [ "orbitofrontal cortex" ], "offsets": [ [ 4633, 4653 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T15", "type": "Multi-tissue_structure", "text": [ "ventral" ], "offsets": [ [ 4664, 4671 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T16", "type": "Multi-tissue_structure", "text": [ "dorsal striatum" ], "offsets": [ [ 4676, 4691 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T17", "type": "Multi-tissue_structure", "text": [ "nucleus accumbens" ], "offsets": [ [ 4693, 4710 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T18", "type": "Multi-tissue_structure", "text": [ "putamen" ], "offsets": [ [ 4712, 4719 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T19", "type": "Multi-tissue_structure", "text": [ "caudate" ], "offsets": [ [ 4725, 4732 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T20", "type": "Multi-tissue_structure", "text": [ "oculomotor structure superior colliculus" ], "offsets": [ [ 4800, 4840 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T21", "type": "Multi-tissue_structure", "text": [ "superior colliculus" ], "offsets": [ [ 4889, 4908 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T22", "type": "Multi-tissue_structure", "text": [ "oculomotor" ], "offsets": [ [ 4935, 4945 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T23", "type": "Multi-tissue_structure", "text": [ "oculomotor control system" ], "offsets": [ [ 5281, 5306 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T24", "type": "Multi-tissue_structure", "text": [ "basal ganglia" ], "offsets": [ [ 5333, 5346 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T25", "type": "Multi-tissue_structure", "text": [ "oculomotor network" ], "offsets": [ [ 5359, 5377 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T26", "type": "Multi-tissue_structure", "text": [ "cortical eyefields" ], "offsets": [ [ 5424, 5442 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T27", "type": "Multi-tissue_structure", "text": [ "frontal" ], "offsets": [ [ 5444, 5451 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T28", "type": "Multi-tissue_structure", "text": [ "supplementary" ], "offsets": [ [ 5453, 5466 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T29", "type": "Multi-tissue_structure", "text": [ "parietal eyefields" ], "offsets": [ [ 5472, 5490 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T30", "type": "Multi-tissue_structure", "text": [ "visual cortex" ], "offsets": [ [ 5512, 5525 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T31", "type": "Multi-tissue_structure", "text": [ "frontal eyefields" ], "offsets": [ [ 5588, 5605 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T32", "type": "Multi-tissue_structure", "text": [ "frontal eyefields" ], "offsets": [ [ 5834, 5851 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T33", "type": "Multi-tissue_structure", "text": [ "striatum" ], "offsets": [ [ 5895, 5903 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T34", "type": "Multi-tissue_structure", "text": [ "cerebral cortex" ], "offsets": [ [ 5946, 5961 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T35", "type": "Multi-tissue_structure", "text": [ "reentrant corticobasal ganglia" ], "offsets": [ [ 5978, 6008 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T36", "type": "Multi-tissue_structure", "text": [ "cortical eyefields" ], "offsets": [ [ 6096, 6114 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T37", "type": "Multi-tissue_structure", "text": [ "subcortical" ], "offsets": [ [ 6167, 6178 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T38", "type": "Multi-tissue_structure", "text": [ "oculomotor network" ], "offsets": [ [ 6197, 6215 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T39", "type": "Multi-tissue_structure", "text": [ "caudate" ], "offsets": [ [ 6294, 6301 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T40", "type": "Multi-tissue_structure", "text": [ "subcortical" ], "offsets": [ [ 6336, 6347 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T41", "type": "Multi-tissue_structure", "text": [ "cortical nodes" ], "offsets": [ [ 6362, 6376 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T42", "type": "Multi-tissue_structure", "text": [ "oculomotor network" ], "offsets": [ [ 6384, 6402 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T43", "type": "Cell", "text": [ "spiny projection neurons" ], "offsets": [ [ 6594, 6618 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T44", "type": "Multi-tissue_structure", "text": [ "striatum" ], "offsets": [ [ 6626, 6634 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T45", "type": "Multi-tissue_structure", "text": [ "oculomotor" ], "offsets": [ [ 6909, 6919 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T46", "type": "Multi-tissue_structure", "text": [ "cortex" ], "offsets": [ [ 7067, 7073 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T47", "type": "Multi-tissue_structure", "text": [ "basal ganglia" ], "offsets": [ [ 7194, 7207 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T48", "type": "Multi-tissue_structure", "text": [ "speed motor" ], "offsets": [ [ 7225, 7236 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T49", "type": "Cell", "text": [ "caudate projection neurons" ], "offsets": [ [ 7396, 7422 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T50", "type": "Cell", "text": [ "neurons" ], "offsets": [ [ 7933, 7940 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T51", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 9014, 9020 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T52", "type": "Multi-tissue_structure", "text": [ "striatum" ], "offsets": [ [ 9067, 9075 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T53", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 9185, 9191 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T54", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 9508, 9514 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T55", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 9941, 9947 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T56", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 9996, 10002 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T57", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 10732, 10738 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T58", "type": "Multi-tissue_structure", "text": [ "oculomotor" ], "offsets": [ [ 11436, 11446 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T59", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 11688, 11694 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T60", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 11791, 11797 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T61", "type": "Anatomical_system", "text": [ "neural systems" ], "offsets": [ [ 11868, 11882 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T62", "type": "Anatomical_system", "text": [ "action control system" ], "offsets": [ [ 11896, 11917 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T63", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 12040, 12045 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T64", "type": "Multi-tissue_structure", "text": [ "neural network" ], "offsets": [ [ 12148, 12162 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T65", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 12205, 12210 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T66", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 12334, 12339 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T67", "type": "Multi-tissue_structure", "text": [ "frontostriatal" ], "offsets": [ [ 12386, 12400 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T68", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 12717, 12723 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T69", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 13520, 13526 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T70", "type": "Multi-tissue_structure", "text": [ "oculomotor-control networks" ], "offsets": [ [ 14584, 14611 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T71", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 14619, 14624 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T72", "type": "Multi-tissue_structure", "text": [ "dorsal striatum" ], "offsets": [ [ 14674, 14689 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T73", "type": "Multi-tissue_structure", "text": [ "oculomotor" ], "offsets": [ [ 14749, 14759 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T74", "type": "Multi-tissue_structure", "text": [ "caudate" ], "offsets": [ [ 15110, 15117 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T75", "type": "Multi-tissue_structure", "text": [ "neural" ], "offsets": [ [ 15296, 15302 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T76", "type": "Multi-tissue_structure", "text": [ "caudate" ], "offsets": [ [ 5819, 5826 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T77", "type": "Multi-tissue_structure", "text": [ "caudate" ], "offsets": [ [ 7903, 7910 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T78", "type": "Multi-tissue_structure", "text": [ "oculomotor" ], "offsets": [ [ 14482, 14492 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T79", "type": "Multi-tissue_structure", "text": [ "striatal" ], "offsets": [ [ 6718, 6726 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T80", "type": "Multi-tissue_structure", "text": [ "striatal" ], "offsets": [ [ 7543, 7551 ] ], "normalized": [] }, { "id": "PMC-2972690-sec-19_T81", "type": "Multi-tissue_structure", "text": [ "striatal" ], "offsets": [ [ 14254, 14262 ] ], "normalized": [] } ]
[]
[]
[ { "id": "PMC-2972690-sec-19_R1", "type": "frag", "arg1_id": "PMC-2972690-sec-19_T15", "arg2_id": "PMC-2972690-sec-19_T16", "normalized": [] }, { "id": "PMC-2972690-sec-19_R2", "type": "frag", "arg1_id": "PMC-2972690-sec-19_T28", "arg2_id": "PMC-2972690-sec-19_T29", "normalized": [] }, { "id": "PMC-2972690-sec-19_R3", "type": "frag", "arg1_id": "PMC-2972690-sec-19_T27", "arg2_id": "PMC-2972690-sec-19_T29", "normalized": [] }, { "id": "PMC-2972690-sec-19_R4", "type": "Part-of", "arg1_id": "PMC-2972690-sec-19_T70", "arg2_id": "PMC-2972690-sec-19_T71", "normalized": [] } ]
PMID-1517352
PMID-1517352
[ { "id": "PMID-1517352__text", "type": "abstract", "text": [ "Active respiratory syncytial virus purified by ion-exchange chromatography: characterization of binding and elution requirements.\nTwo viruses, respiratory syncytial virus (RSV) and vesicular stomatitis virus (VSV) were used to evaluate viral purification by an affinity resin column (Matrex Cellufine Sulfate (MCS); Amicon Division, WR Grace & Co.). Viable RSV was purified significantly from crude cell lysate by a single pass through a column containing the anionic MCS resin. Most cell protein and albumin eluted from the MCS resin with phosphate buffered saline (PBS) but RSV eluted at high ionic strength, i.e., greater than or equal to 0.6 M NaCl. Further purification was possible by sucrose step gradient centrifugation. The RSV prepared by column purification or by column plus sucrose gradient separation was both intact and infective. RSV and pure samples of VSV were used to optimize ionic strength and salts for elution from the MCS column: 0.8 M NaCl removed most of the viral protein. The capacity of the MCS gel for RSV or VSV was found to be about 0.6-0.8 mg viral protein per ml of hydrated resin. Detergent-solubilized viral membrane proteins bound to the MCS resin in 0.145 M NaCl and eluted with higher salt concentrations. Thus, this resin also may be a useful aid for relatively gentle purification of these proteins.\n" ], "offsets": [ [ 0, 1341 ] ] } ]
[ { "id": "PMID-1517352_T4", "type": "Organism_substance", "text": [ "cell lysate" ], "offsets": [ [ 399, 410 ] ], "normalized": [] }, { "id": "PMID-1517352_T5", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 484, 488 ] ], "normalized": [] }, { "id": "PMID-1517352_T6", "type": "Cellular_component", "text": [ "membrane" ], "offsets": [ [ 1144, 1152 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2648768-caption-01
PMC-2648768-caption-01
[ { "id": "PMC-2648768-caption-01__text", "type": "caption", "text": [ "Power (Y-axis) as a function of main effects (x-axis). For a pure main-effects model (x-axis = a1 > 0; interaction effects a2 = a3 = 0 are all zero), Figure 1 shows that pattern (solid red line) and single-locus (broken blue line) approaches have virtually the same power.\n" ], "offsets": [ [ 0, 273 ] ] } ]
[]
[]
[]
[]
PMID-8078269
PMID-8078269
[ { "id": "PMID-8078269__text", "type": "abstract", "text": [ "[Preliminary results of observing 18 cases of retinoblastoma carried within the international research program RICS].\nIn the years 1988-1989, the Ophthalmological Clinic in Cracow took part in the International Research Programme on Retinoblastoma as one of 28 clinical centres in 14 countries. The study included 18 children with retinoblastoma, in most cases in the advanced stadium of the disease. As a rule, the eyes filled with tumours were enucleated, and the less advanced cases were treated with combined methods applying radiation with 60Co plaques with xenon arc photocoagulation, cryopexy, and chemotherapy. In 18 treated children 23 eyes were enucleated (in 5 children both eyes, in 6 children with bilateral retinoblastoma 1 eye, and 7 eyes in all unilateral cases). Six eyes with less advanced lesions were treated with combined methods. One child died because of metastases to the brain. The obtained data reveal that retinoblastoma is diagnosed too late, which decreases the chance of cure and causes great danger for the life of the child.\n" ], "offsets": [ [ 0, 1057 ] ] } ]
[ { "id": "PMID-8078269_T1", "type": "Pathological_formation", "text": [ "retinoblastoma" ], "offsets": [ [ 46, 60 ] ], "normalized": [] }, { "id": "PMID-8078269_T2", "type": "Pathological_formation", "text": [ "Retinoblastoma" ], "offsets": [ [ 233, 247 ] ], "normalized": [] }, { "id": "PMID-8078269_T3", "type": "Pathological_formation", "text": [ "retinoblastoma" ], "offsets": [ [ 331, 345 ] ], "normalized": [] }, { "id": "PMID-8078269_T4", "type": "Pathological_formation", "text": [ "retinoblastoma" ], "offsets": [ [ 721, 735 ] ], "normalized": [] }, { "id": "PMID-8078269_T5", "type": "Organ", "text": [ "eye" ], "offsets": [ [ 738, 741 ] ], "normalized": [] }, { "id": "PMID-8078269_T6", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 749, 753 ] ], "normalized": [] }, { "id": "PMID-8078269_T7", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 784, 788 ] ], "normalized": [] }, { "id": "PMID-8078269_T8", "type": "Organ", "text": [ "brain" ], "offsets": [ [ 896, 901 ] ], "normalized": [] }, { "id": "PMID-8078269_T9", "type": "Pathological_formation", "text": [ "retinoblastoma" ], "offsets": [ [ 933, 947 ] ], "normalized": [] }, { "id": "PMID-8078269_T10", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 645, 649 ] ], "normalized": [] }, { "id": "PMID-8078269_T11", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 686, 690 ] ], "normalized": [] }, { "id": "PMID-8078269_T12", "type": "Organ", "text": [ "eyes" ], "offsets": [ [ 416, 420 ] ], "normalized": [] }, { "id": "PMID-8078269_T13", "type": "Pathological_formation", "text": [ "tumours" ], "offsets": [ [ 433, 440 ] ], "normalized": [] }, { "id": "PMID-8078269_T14", "type": "Pathological_formation", "text": [ "lesions" ], "offsets": [ [ 808, 815 ] ], "normalized": [] }, { "id": "PMID-8078269_T15", "type": "Pathological_formation", "text": [ "metastases" ], "offsets": [ [ 878, 888 ] ], "normalized": [] } ]
[]
[]
[]
PMID-16969171
PMID-16969171
[ { "id": "PMID-16969171__text", "type": "abstract", "text": [ "Medical adherence and childhood chronic illness: family daily management skills and emotional climate as emerging contributors.\nPURPOSE OF REVIEW:\nTo describe recent research that examines family factors that promote or derail adherence to medical regimens for children with chronic health conditions, primarily asthma, diabetes, and cystic fibrosis. From the past 2 years, eight correlational studies were identified which specifically examined the links between family management strategies, family climate and medical adherence.\nRECENT FINDINGS:\nFindings from the studies suggest that team-based management strategies and cohesive family climate promote adherence to medical treatments over time. Family interactions that are characterized by conflict and disengagement tend to disrupt adherence and inevitably cause a decline in child health. Moreover, these findings seem to be moderated by child age in that poorer adherence often occurs when a child reaches adolescence and is searching for greater autonomy.\nSUMMARY:\nFuture research should consider the challenges in measuring medical adherence in the family context as well as incorporating more naturalistic studies of family interactions. Randomized controlled trials using family-based interventions may consider focusing on medical adherence as an important mediator between family process and child health outcomes.\n" ], "offsets": [ [ 0, 1380 ] ] } ]
[]
[]
[]
[]
PMC-2892686-caption-01
PMC-2892686-caption-01
[ { "id": "PMC-2892686-caption-01__text", "type": "caption", "text": [ "Large nodular hepatic flexure lesions as seen on Colonoscopy.\n" ], "offsets": [ [ 0, 62 ] ] } ]
[ { "id": "PMC-2892686-caption-01_T1", "type": "Pathological_formation", "text": [ "nodular hepatic flexure lesions" ], "offsets": [ [ 6, 37 ] ], "normalized": [] } ]
[]
[]
[]
PMC-3113832-caption-05
PMC-3113832-caption-05
[ { "id": "PMC-3113832-caption-05__text", "type": "caption", "text": [ "Concurrent disease in 33 cows with LDA.\n" ], "offsets": [ [ 0, 40 ] ] } ]
[]
[]
[]
[]
PMID-8925114
PMID-8925114
[ { "id": "PMID-8925114__text", "type": "abstract", "text": [ "Functional model of benign paroxysmal positional vertigo using an isolated frog semicircular canal.\nBull frogs posterior semicircular canals (psc) wee used to simulate the condition of benign paroxysmal positional vertigo (BPPV). The psc was isolated in frog Ringer's solution, and the saccular otoconia were used as a responsible material to stimulate the cupula. When the otoconia were placed on the cupular surface to mimic the condition of cupulolithiasis, the psc ampullary nerve action potentials instantaneously changed according to the direction of the gravity produced by otoconia. When the otoconia were dropped into the canal to mimic the condition of moving otoconia in the canal, the action potentials changed together with the otoconial flow after a latent period. Both cupulolithiasis and moving otoconia are possibly valid mechanisms of BPPV, since they effectively stimulate the cupula. However, moving otoconia with a latent period would better explain clinical features of BPPV.\n" ], "offsets": [ [ 0, 998 ] ] } ]
[ { "id": "PMID-8925114_T1", "type": "Multi-tissue_structure", "text": [ "semicircular canal" ], "offsets": [ [ 80, 98 ] ], "normalized": [] }, { "id": "PMID-8925114_T2", "type": "Multi-tissue_structure", "text": [ "posterior semicircular canals" ], "offsets": [ [ 111, 140 ] ], "normalized": [] }, { "id": "PMID-8925114_T3", "type": "Multi-tissue_structure", "text": [ "psc" ], "offsets": [ [ 142, 145 ] ], "normalized": [] }, { "id": "PMID-8925114_T4", "type": "Multi-tissue_structure", "text": [ "psc" ], "offsets": [ [ 234, 237 ] ], "normalized": [] }, { "id": "PMID-8925114_T5", "type": "Organism_substance", "text": [ "saccular otoconia" ], "offsets": [ [ 286, 303 ] ], "normalized": [] }, { "id": "PMID-8925114_T6", "type": "Multi-tissue_structure", "text": [ "cupula" ], "offsets": [ [ 357, 363 ] ], "normalized": [] }, { "id": "PMID-8925114_T7", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 374, 382 ] ], "normalized": [] }, { "id": "PMID-8925114_T8", "type": "Multi-tissue_structure", "text": [ "cupular surface" ], "offsets": [ [ 402, 417 ] ], "normalized": [] }, { "id": "PMID-8925114_T9", "type": "Multi-tissue_structure", "text": [ "psc ampullary nerve" ], "offsets": [ [ 465, 484 ] ], "normalized": [] }, { "id": "PMID-8925114_T10", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 581, 589 ] ], "normalized": [] }, { "id": "PMID-8925114_T11", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 600, 608 ] ], "normalized": [] }, { "id": "PMID-8925114_T12", "type": "Multi-tissue_structure", "text": [ "canal" ], "offsets": [ [ 631, 636 ] ], "normalized": [] }, { "id": "PMID-8925114_T13", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 670, 678 ] ], "normalized": [] }, { "id": "PMID-8925114_T14", "type": "Multi-tissue_structure", "text": [ "canal" ], "offsets": [ [ 686, 691 ] ], "normalized": [] }, { "id": "PMID-8925114_T15", "type": "Organism_substance", "text": [ "otoconial" ], "offsets": [ [ 741, 750 ] ], "normalized": [] }, { "id": "PMID-8925114_T16", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 811, 819 ] ], "normalized": [] }, { "id": "PMID-8925114_T17", "type": "Multi-tissue_structure", "text": [ "cupula" ], "offsets": [ [ 896, 902 ] ], "normalized": [] }, { "id": "PMID-8925114_T18", "type": "Organism_substance", "text": [ "otoconia" ], "offsets": [ [ 920, 928 ] ], "normalized": [] } ]
[]
[ { "id": "PMID-8925114_1", "entity_ids": [ "PMID-8925114_T2", "PMID-8925114_T3" ] } ]
[]
PMC-3249382-caption-01
PMC-3249382-caption-01
[ { "id": "PMC-3249382-caption-01__text", "type": "caption", "text": [ "Predicted methylation level of C. gigas genes categorized by biological processes compared to measured level of DNA methylation. Mean CpG O/E for 10,699 C. gigas genes categorized according to Biological Process Gene Ontology (GO) Slim terms are plotted on the x-axis (modified from Gavery and Roberts, 2010). DNA methylation was empirically measured by performing MBD-seq on the SOLiD 4 platform (Applied Biosystems). Genes identified in the MBD-library were associated with respective GO terms and enrichment analysis was performed based on the entire transcriptome (Fleury et al., 2009) using DAVID (Huang et al., 2009a,b). Results indicate the most underrepresented genes in the library are involved in cell adhesion and genes involved in DNA and protein metabolism were most prevalent in the MBD-library.\n" ], "offsets": [ [ 0, 810 ] ] } ]
[ { "id": "PMC-3249382-caption-01_T1", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 707, 711 ] ], "normalized": [] } ]
[]
[]
[]
PMID-21617625
PMID-21617625
[ { "id": "PMID-21617625__text", "type": "abstract", "text": [ "Non-heart-beating organ donation in Italy.\nIn 2007 the non-heart-beating organ donation (NHBD) \"Programma Alba\" (Sunrise Programme) started in Pavia, Italy. The initial plan was to cut down waiting list for kidney transplantation, while its final aim is to shorten organ transplantation waiting lists. When compared to European countries and the USA, the Italian NHBD program has taken longer to get established. Initially Italian physicians were not entirely aware of the NHBD organ viability for transplantation, furthermore ethical issues and the need to regulate medical requirements to Italian law slowed down the NHBD program. In particular, Italian legislation provides for death ascertainment after irreversible cardiac arrest, 20-minute flat electrocardiogram. This no-touch period is longer when compared to worldwide legislation, and organ viability has been a main concern for Italian transplant doctors over the years. However, recent data let up to 40-minute warm ischemia time to preserve organ viability; this has encouraged Pavia's group to establish the NHBD \"Programma Alba\". It was designed according to Italian legislation from death diagnosis to graft placement, from this perspective must the significant role of the Transplant coordinator be recognized. Since 2007 seven kidneys have been gathered from seven NHBD. Of these, six NHBD kidneys have been transplanted. Currently, four patients are out of dialysis. This report is a detailed description of NHBD \"Programma Alba\" and its preliminary results.\n" ], "offsets": [ [ 0, 1528 ] ] } ]
[ { "id": "PMID-21617625_T1", "type": "Organ", "text": [ "heart" ], "offsets": [ [ 4, 9 ] ], "normalized": [] }, { "id": "PMID-21617625_T2", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 18, 23 ] ], "normalized": [] }, { "id": "PMID-21617625_T3", "type": "Organ", "text": [ "heart" ], "offsets": [ [ 59, 64 ] ], "normalized": [] }, { "id": "PMID-21617625_T4", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 73, 78 ] ], "normalized": [] }, { "id": "PMID-21617625_T5", "type": "Organ", "text": [ "kidney" ], "offsets": [ [ 207, 213 ] ], "normalized": [] }, { "id": "PMID-21617625_T6", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 265, 270 ] ], "normalized": [] }, { "id": "PMID-21617625_T7", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 478, 483 ] ], "normalized": [] }, { "id": "PMID-21617625_T8", "type": "Organ", "text": [ "cardiac" ], "offsets": [ [ 720, 727 ] ], "normalized": [] }, { "id": "PMID-21617625_T9", "type": "Organ", "text": [ "graft" ], "offsets": [ [ 1168, 1173 ] ], "normalized": [] }, { "id": "PMID-21617625_T10", "type": "Organ", "text": [ "kidneys" ], "offsets": [ [ 1295, 1302 ] ], "normalized": [] }, { "id": "PMID-21617625_T11", "type": "Organ", "text": [ "kidneys" ], "offsets": [ [ 1358, 1365 ] ], "normalized": [] }, { "id": "PMID-21617625_T12", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 1004, 1009 ] ], "normalized": [] }, { "id": "PMID-21617625_T13", "type": "Organ", "text": [ "organ" ], "offsets": [ [ 845, 850 ] ], "normalized": [] } ]
[]
[]
[]
PMID-15542670
PMID-15542670
[ { "id": "PMID-15542670__text", "type": "abstract", "text": [ "Human cytomegalovirus 5-kilobase immediate-early RNA is a stable intron.\nImmediate-early viral gene products of human cytomegalovirus (HCMV) are derived from several genomic loci and largely serve to establish a cellular environment conducive to viral replication. We have further examined an unusual immediate-early transcript known as the 5-kb RNA, concluding that it is a stable intron encoded by HCMV. The 5-kb RNA is highly AT rich in sequence and lacks open reading frames likely to be translated into protein. We confirmed the absence of polyadenylation of the transcript and showed that it is primarily nuclear localized during viral infection. We mapped the 5' end of the 5-kb RNA to a consensus splice donor site and localized the 3' end in the vicinity of a splice acceptor site. In transfection studies, we showed that the 5-kb RNA can be spliced from a heterologous primary transcript. Using bacterial artificial chromosome technology, we constructed a viral recombinant containing a mutation in the 5' splice donor site that defines the 5' end of the RNA and found that this mutation eliminates expression of the 5-kb RNA during viral infection. This mutant grows in human fibroblasts without complementation. Taken together, these data support the conclusion that the 5-kb RNA is a stable intron expressed by HCMV.\n" ], "offsets": [ [ 0, 1330 ] ] } ]
[ { "id": "PMID-15542670_T1", "type": "Cellular_component", "text": [ "nuclear" ], "offsets": [ [ 611, 618 ] ], "normalized": [] }, { "id": "PMID-15542670_T2", "type": "Cellular_component", "text": [ "chromosome" ], "offsets": [ [ 926, 936 ] ], "normalized": [] }, { "id": "PMID-15542670_T3", "type": "Cell", "text": [ "fibroblasts" ], "offsets": [ [ 1187, 1198 ] ], "normalized": [] }, { "id": "PMID-15542670_T4", "type": "Cell", "text": [ "cellular" ], "offsets": [ [ 212, 220 ] ], "normalized": [] } ]
[]
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PMID-8898364
PMID-8898364
[ { "id": "PMID-8898364__text", "type": "abstract", "text": [ "Induction of p18INK4c and its predominant association with CDK4 and CDK6 during myogenic differentiation.\nTerminal cell differentiation involves permanent withdrawal from the cell division cycle. The inhibitors of cyclin-dependent kinases (CDKs) are potential molecules functioning to couple cell cycle arrest and cell differentiation. In murine C2C12 myoblast cells, G1 CDK enzymes (CDK2, CDK4, and CDK6) associate with four CDK inhibitors: p18INK4c, p19INK4d, p21, and p27Kip1. During induced myogenesis, p21 and its associated CDK proteins underwent an initial increase followed by a decrease as cells became terminally differentiated. The level of p27 protein gradually increased, but the amount of total associated CDK proteins remained unchanged. p19 protein decreased gradually during differentiation, as did its associated CDK4 protein. In contrast, p18 protein increased 50-fold, from negligible levels in proliferating myoblasts to clearly detectable levels within 8-12 h of myogenic induction. This initial rise was followed by a precipitous increase between 12 and 24 h postinduction, with p18 protein finally accumulating to its highest level in terminally differentiated cells. Induction of p18 correlated with increased and sequential complex formation--first increasing association with CDK6 and then with CDK4 over the course of myogenic differentiation. All of the CDK6 and half of the CDK4 were complexed with p18 in terminally differentiated C2C12 cells as well as in adult mouse muscle tissue. Finally, kinase activity of CDK2 and CDK4 decreases as C2C12 cells differentiate, whereas the CDK6 kinase activity is low in both proliferating myoblasts and differentiated myotubes. Our results indicate that p18 may play a critical role in causing and/or maintaining permanent cell cycle arrest associated with mature muscle formation.\n" ], "offsets": [ [ 0, 1852 ] ] } ]
[ { "id": "PMID-8898364_T1", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 115, 119 ] ], "normalized": [] }, { "id": "PMID-8898364_T2", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 175, 179 ] ], "normalized": [] }, { "id": "PMID-8898364_T3", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 292, 296 ] ], "normalized": [] }, { "id": "PMID-8898364_T4", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 314, 318 ] ], "normalized": [] }, { "id": "PMID-8898364_T5", "type": "Cell", "text": [ "C2C12 myoblast cells" ], "offsets": [ [ 346, 366 ] ], "normalized": [] }, { "id": "PMID-8898364_T6", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 599, 604 ] ], "normalized": [] }, { "id": "PMID-8898364_T7", "type": "Cell", "text": [ "cells" ], "offsets": [ [ 1185, 1190 ] ], "normalized": [] }, { "id": "PMID-8898364_T8", "type": "Cell", "text": [ "C2C12 cells" ], "offsets": [ [ 1462, 1473 ] ], "normalized": [] }, { "id": "PMID-8898364_T9", "type": "Tissue", "text": [ "muscle tissue" ], "offsets": [ [ 1500, 1513 ] ], "normalized": [] }, { "id": "PMID-8898364_T10", "type": "Cell", "text": [ "C2C12 cells" ], "offsets": [ [ 1570, 1581 ] ], "normalized": [] }, { "id": "PMID-8898364_T11", "type": "Cell", "text": [ "myoblasts" ], "offsets": [ [ 1659, 1668 ] ], "normalized": [] }, { "id": "PMID-8898364_T12", "type": "Tissue", "text": [ "myotubes" ], "offsets": [ [ 1688, 1696 ] ], "normalized": [] }, { "id": "PMID-8898364_T13", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 1793, 1797 ] ], "normalized": [] }, { "id": "PMID-8898364_T14", "type": "Tissue", "text": [ "muscle" ], "offsets": [ [ 1834, 1840 ] ], "normalized": [] }, { "id": "PMID-8898364_T15", "type": "Cell", "text": [ "myoblasts" ], "offsets": [ [ 929, 938 ] ], "normalized": [] } ]
[]
[]
[]
PMID-8455978
PMID-8455978
[ { "id": "PMID-8455978__text", "type": "abstract", "text": [ "[Prehospital service in Denmark].\nIn Denmark, emergency ambulances are dispatched by 41 centres manned either by trained firemen (in Copenhagen) or policemen (outside Copenhagen). In 1990, emergency ambulance calls totalled 284,000. Utilisation of emergency ambulance services increases with urbanisation. A doctor-manned ambulance is in operation in Copenhagen, and in some other large towns anaesthesiology and intensive care teams can be dispatched from hospital to give on-the-spot care. In less populated areas, some general practitioners give advanced life-support. Although many areas are serviced by ambulances equipped with defibrillators, the majority of patients receive only basic life-support from ambulance personnel. New initiatives resulting from a recent report by a commission appointed by central authorities, and focused on prehospital treatment, are expected to improve the service by raising the level of training given to ambulance personnel.\n" ], "offsets": [ [ 0, 966 ] ] } ]
[]
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PMC-2673029-caption-03
PMC-2673029-caption-03
[ { "id": "PMC-2673029-caption-03__text", "type": "caption", "text": [ "Secchi depth in the Baltic Proper, June-August, 1957-1998.\nNumber of data: 3,452.\n" ], "offsets": [ [ 0, 82 ] ] } ]
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PMC-2192393-sec-06
PMC-2192393-sec-06
[ { "id": "PMC-2192393-sec-06__text", "type": "sec", "text": [ "Cytology and Histology\nFor semithin sections, embryoid bodies were washed twice in PBS, fixed in 4% paraformaldehyde at 4degreesC overnight, and after dehydration in ethanol were embedded in JB-4 resin (Polysciences, Inc.). 1-4-mum sections were cut with a glass knife. For cytology, the sections were stained with toluidine blue. In cell mixing experiments, the embryoid bodies were prefixed and stained for beta-galactosidase and the sections were counterstained with neutral red. Teratocarcinomas were fixed in Bouin fixative, embedded in Paraplast, and the sections were stained with hematoxylin and eosin. Microphotography was with a ZEISS Axiomat microscope. Films were scanned and figures were prepared with Photoshop 5.5 software.\n" ], "offsets": [ [ 0, 739 ] ] } ]
[ { "id": "PMC-2192393-sec-06_T1", "type": "Developing_anatomical_structure", "text": [ "embryoid bodies" ], "offsets": [ [ 46, 61 ] ], "normalized": [] }, { "id": "PMC-2192393-sec-06_T2", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 334, 338 ] ], "normalized": [] }, { "id": "PMC-2192393-sec-06_T3", "type": "Developing_anatomical_structure", "text": [ "embryoid bodies" ], "offsets": [ [ 363, 378 ] ], "normalized": [] } ]
[]
[]
[]
PMC-2840784-sec-02
PMC-2840784-sec-02
[ { "id": "PMC-2840784-sec-02__text", "type": "sec", "text": [ "CASE:\nHere for the first time a case of CDLS from Iran, a 15-week-old male infant who was refereed as a case of multiple congenital anomalies. Clinical investigation showed that the child was a case of CDLS.\n" ], "offsets": [ [ 0, 208 ] ] } ]
[]
[]
[]
[]
PMC-2579698-caption-02
PMC-2579698-caption-02
[ { "id": "PMC-2579698-caption-02__text", "type": "caption", "text": [ "Characteristics of cases with childhood leukaemia (n=162) and matched controls (n=2125), all registered within 3 months of birth\n" ], "offsets": [ [ 0, 129 ] ] } ]
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[]
PMID-7257720
PMID-7257720
[ { "id": "PMID-7257720__text", "type": "abstract", "text": [ "[Organization of pectoral muscle motor neurons in the rat. Contribution to the study of the axillary arch (Achselbogen)].\nIn spite of their role of the forelimb activity, the organization of the mammalian pectoral muscles remains unclear. In order to get more information, we have studied, qualitatively and quantitatively, the motor pools of the various pectoral muscles in the rat (musculus pectoralis major, musculus pectoralis minor and musculus panniculus carnosus). The method applied was the retrograde transport of horseradish peroxidase by the peripheral nerves supplying the various muscles. The results provided the precise localization within the ventral horn of the motor neurons from the pectoral muscles which were all in the most ventral part of the gray matter. Three distinct motor pools were observed, which confirms the functional identity of each muscle. The motor neurons of m. panniculus carnosus exhibited some particularities. They were 4 times more numerous than those from m. pectoralis major, they occupied the whole ventral edge of the ventral horn, from its medial part to its lateral tip. The cell size was different from that of the other muscles. These results were discussed, according to the role of this muscle, which links the forelimb to the whole trunk. In mammals, m. panniculus carnosus constitutes, with musculus latissimus dorsi, the axillary arch (Achselbogen). A small area of overlapping between the motor pools of these two muscles was observed. It was suggested that the muscular fibers from the axillary arch were innervated by the same, well-defined spinal area, independent of the muscle from which they originate.\n" ], "offsets": [ [ 0, 1666 ] ] } ]
[ { "id": "PMID-7257720_T1", "type": "Cell", "text": [ "pectoral muscle motor neurons" ], "offsets": [ [ 17, 46 ] ], "normalized": [] }, { "id": "PMID-7257720_T2", "type": "Organism_subdivision", "text": [ "forelimb" ], "offsets": [ [ 152, 160 ] ], "normalized": [] }, { "id": "PMID-7257720_T3", "type": "Organ", "text": [ "pectoral muscles" ], "offsets": [ [ 205, 221 ] ], "normalized": [] }, { "id": "PMID-7257720_T4", "type": "Organ", "text": [ "pectoral muscles" ], "offsets": [ [ 355, 371 ] ], "normalized": [] }, { "id": "PMID-7257720_T5", "type": "Organ", "text": [ "musculus pectoralis major" ], "offsets": [ [ 384, 409 ] ], "normalized": [] }, { "id": "PMID-7257720_T6", "type": "Organ", "text": [ "musculus pectoralis minor" ], "offsets": [ [ 411, 436 ] ], "normalized": [] }, { "id": "PMID-7257720_T7", "type": "Organ", "text": [ "musculus panniculus carnosus" ], "offsets": [ [ 441, 469 ] ], "normalized": [] }, { "id": "PMID-7257720_T8", "type": "Multi-tissue_structure", "text": [ "peripheral nerves" ], "offsets": [ [ 553, 570 ] ], "normalized": [] }, { "id": "PMID-7257720_T9", "type": "Organ", "text": [ "muscles" ], "offsets": [ [ 593, 600 ] ], "normalized": [] }, { "id": "PMID-7257720_T10", "type": "Cellular_component", "text": [ "ventral horn" ], "offsets": [ [ 659, 671 ] ], "normalized": [] }, { "id": "PMID-7257720_T11", "type": "Cell", "text": [ "motor neurons" ], "offsets": [ [ 679, 692 ] ], "normalized": [] }, { "id": "PMID-7257720_T12", "type": "Organ", "text": [ "pectoral muscles" ], "offsets": [ [ 702, 718 ] ], "normalized": [] }, { "id": "PMID-7257720_T13", "type": "Multi-tissue_structure", "text": [ "gray matter" ], "offsets": [ [ 766, 777 ] ], "normalized": [] }, { "id": "PMID-7257720_T14", "type": "Organ", "text": [ "muscle" ], "offsets": [ [ 868, 874 ] ], "normalized": [] }, { "id": "PMID-7257720_T15", "type": "Cell", "text": [ "motor neurons" ], "offsets": [ [ 880, 893 ] ], "normalized": [] }, { "id": "PMID-7257720_T17", "type": "Cellular_component", "text": [ "ventral edge" ], "offsets": [ [ 1045, 1057 ] ], "normalized": [] }, { "id": "PMID-7257720_T18", "type": "Cellular_component", "text": [ "ventral horn" ], "offsets": [ [ 1065, 1077 ] ], "normalized": [] }, { "id": "PMID-7257720_T19", "type": "Cell", "text": [ "cell" ], "offsets": [ [ 1124, 1128 ] ], "normalized": [] }, { "id": "PMID-7257720_T20", "type": "Organ", "text": [ "muscles" ], "offsets": [ [ 1171, 1178 ] ], "normalized": [] }, { "id": "PMID-7257720_T21", "type": "Organ", "text": [ "muscle" ], "offsets": [ [ 1240, 1246 ] ], "normalized": [] }, { "id": "PMID-7257720_T22", "type": "Organism_subdivision", "text": [ "forelimb" ], "offsets": [ [ 1264, 1272 ] ], "normalized": [] }, { "id": "PMID-7257720_T23", "type": "Organism_subdivision", "text": [ "trunk" ], "offsets": [ [ 1286, 1291 ] ], "normalized": [] }, { "id": "PMID-7257720_T24", "type": "Organ", "text": [ "muscles" ], "offsets": [ [ 1471, 1478 ] ], "normalized": [] }, { "id": "PMID-7257720_T25", "type": "Cell", "text": [ "muscular fibers" ], "offsets": [ [ 1519, 1534 ] ], "normalized": [] }, { "id": "PMID-7257720_T26", "type": "Organ", "text": [ "musculus latissimus dorsi" ], "offsets": [ [ 1346, 1371 ] ], "normalized": [] }, { "id": "PMID-7257720_T27", "type": "Multi-tissue_structure", "text": [ "axillary arch" ], "offsets": [ [ 1377, 1390 ] ], "normalized": [] }, { "id": "PMID-7257720_T28", "type": "Multi-tissue_structure", "text": [ "axillary arch" ], "offsets": [ [ 1544, 1557 ] ], "normalized": [] }, { "id": "PMID-7257720_T29", "type": "Organ", "text": [ "muscle" ], "offsets": [ [ 1632, 1638 ] ], "normalized": [] }, { "id": "PMID-7257720_T30", "type": "Multi-tissue_structure", "text": [ "ventral part" ], "offsets": [ [ 746, 758 ] ], "normalized": [] }, { "id": "PMID-7257720_T32", "type": "Organism_subdivision", "text": [ "spinal area" ], "offsets": [ [ 1600, 1611 ] ], "normalized": [] }, { "id": "PMID-7257720_T16", "type": "Multi-tissue_structure", "text": [ "axillary arch" ], "offsets": [ [ 92, 105 ] ], "normalized": [] } ]
[]
[]
[ { "id": "PMID-7257720_R1", "type": "Part-of", "arg1_id": "PMID-7257720_T30", "arg2_id": "PMID-7257720_T13", "normalized": [] } ]
PMC-2634619-caption-01
PMC-2634619-caption-01
[ { "id": "PMC-2634619-caption-01__text", "type": "caption", "text": [ "Appendix Table\nDetection of Nipah virus antibody among bat serum samples collected from 10 provinces in China, 2004-2007*\n" ], "offsets": [ [ 0, 122 ] ] } ]
[ { "id": "PMC-2634619-caption-01_T1", "type": "Organism_substance", "text": [ "serum samples" ], "offsets": [ [ 59, 72 ] ], "normalized": [] } ]
[]
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