id
stringlengths 11
22
| document_id
stringlengths 11
22
| passages
list | entities
list | events
list | coreferences
list | relations
list |
|---|---|---|---|---|---|---|
PMID-7511490 | PMID-7511490 | [
{
"id": "PMID-7511490__text",
"type": "abstract",
"text": [
"Additional tests of interest to the dermatologist.\nThe carcinoid syndrome and its clinical manifestations have been discussed. The standard laboratory test for making that diagnosis is urinary 5-HIAA levels but newer, more sensitive tests may also be available.\n"
],
"offsets": [
[
0,
262
]
]
}
] | [
{
"id": "PMID-7511490_T1",
"type": "Organism_substance",
"text": [
"urinary"
],
"offsets": [
[
185,
192
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3173373-caption-02 | PMC-3173373-caption-02 | [
{
"id": "PMC-3173373-caption-02__text",
"type": "caption",
"text": [
"Parameters derived from normalized averaged data across participants\n"
],
"offsets": [
[
0,
69
]
]
}
] | [] | [] | [] | [] |
PMC-2837610-sec-05 | PMC-2837610-sec-05 | [
{
"id": "PMC-2837610-sec-05__text",
"type": "sec",
"text": [
"1. Background\nThe United Republic of Tanzania, is among the many countries in sub-Saharan Africa facing a human resources crisis in its health sector, with a small and inequitably distributed health workforce [1] that shoulders a disproportionately high burden of disease[2]. Although all poor countries in the world face a severe human resource crisis in their health sectors [3,4], the problem is most acute in Sub-Saharan Africa, in which an estimated workforce of 750 000 health workers in the region serves 682 million people [2]. By comparison, the ratio is 10 to 15 times higher in developed countries. Moreover, this estimated workforce of doctors, nurses and allied health workers in Sub-Saharan Africa constitutes 1.3% of the world's health workforce, while Africa suffers from 25% of the world's burden of disease [2].\nA minimum level of a health workforce of 2.5 health workers per 1000 people is required to achieve the Millennium Development Goals [5]. Africa is far from this level with a health workforce density that only averages 0.8 worker per 1000 people, while the world median density of health personnel is 5 per 1000 people [5].\nThere is a positive correlation between health worker density and various health indices, most notably infant mortality rate, maternal mortality rates, and various disease specific mortality and morbidity rates [6,7]. An increase in the number of health workers per capita is associated with a notable decline in the rates mentioned above. As a consequence, it has been argued that health worker shortages have impeded the implementation of development goals in many poor countries [8].\n\n"
],
"offsets": [
[
0,
1641
]
]
}
] | [] | [] | [] | [] |
PMC-3267723-sec-02 | PMC-3267723-sec-02 | [
{
"id": "PMC-3267723-sec-02__text",
"type": "sec",
"text": [
"Results\n\n"
],
"offsets": [
[
0,
9
]
]
}
] | [] | [] | [] | [] |
PMC-2719750-sec-10 | PMC-2719750-sec-10 | [
{
"id": "PMC-2719750-sec-10__text",
"type": "sec",
"text": [
"Quantitative reverse transcription PCR\nReverse transcription was performed using 0.2 mug of total RNA from muscle of 10 week-old and 19 month-old C57Bl6 mice (five animals per group), a Core kit (RT-RTCK-03, Eurogentec) according to manufacturer's instruction and a mix of random primers (9 mers) and oligodT. qPCR was performed on SDS7900HT (Applied Biosystem) using Mesagreen qPCR kit for SYBR (Eurogentec) and the following primers: \nPPARbeta: 5'-AGATGGTGGCAGAGCTATGACC-3'; 5'-TCCTCCTGTGGCTGTTCC-3'.\nCatalase: 5'-GGATCCTGACATGGTCTGGG-3'; 5'-TGGAGAGACTCGGGACGAAG-3'.\nPDK4: 5'-GCATTTCTACTCGGATGCTCAATG-3'; 5'-CCAATGTGGCTTGGGTTTCC-3'.\n36B4: 5'-TCCAGGCTTTGGGCATCA-3'; 5'-CTTTATCAGCTGCACATCACTCAGA-3'.\nData were all normalised using 36B4 as housekeeping gene.\n"
],
"offsets": [
[
0,
758
]
]
}
] | [
{
"id": "PMC-2719750-sec-10_T1",
"type": "Tissue",
"text": [
"muscle"
],
"offsets": [
[
107,
113
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16165242 | PMID-16165242 | [
{
"id": "PMID-16165242__text",
"type": "abstract",
"text": [
"Enhancement of skin permeation of ketotifen by supersaturation generated by amorphous form of the drug.\nPressure sensitive adhesive (PSA) matrices containing amorphous ketotifen were prepared and evaluated for enhanced skin permeability of the drug. A solvent casting method using silicone-typed PSA was employed, and n-hexane, an original solvent for the PSA and one more solvent, dichloromethane, tetrahydrofuran, acetone, ethyl acetate or toluene, were used for complete dissolution of ketotifen and high dispersion in an amorphous state of the drug. Presence of the amorphous form was judged based on the in vitro drug release rate from the matrix. As a result, dichloromethane and tetrahudrofuran were selected as appropriate dilution solvents. In vitro permeation experiments through excised hairless mouse skin revealed that the steady-state flux from the amorphous ketotifen-dispersed matrices was about five times greater than that of the crystalline ketotifen-dispersed matrices, and that the enhancement ratio was in good agreement with the solubility ratio of the amorphous to crystalline form of the drug. Comparison of the skin permeation profiles of amorphous ketotifen-dispersed matrices between two different drug contents suggested that the steady-state flux was not influenced by the drug content. In addition, at both drug contents, the period of the steady-state permeation coincided with the time until the amorphous drug was depleted from the matrix. These results suggest that the increase in skin permeation of ketotifen from PSA matrix was due to the supersaturation generated by amorphous form, and that the amorphous form was stable during the application period.\n"
],
"offsets": [
[
0,
1692
]
]
}
] | [
{
"id": "PMID-16165242_T1",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
15,
19
]
],
"normalized": []
},
{
"id": "PMID-16165242_T2",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
219,
223
]
],
"normalized": []
},
{
"id": "PMID-16165242_T3",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
813,
817
]
],
"normalized": []
},
{
"id": "PMID-16165242_T4",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
1137,
1141
]
],
"normalized": []
},
{
"id": "PMID-16165242_T5",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
1517,
1521
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-21596785 | PMID-21596785 | [
{
"id": "PMID-21596785__text",
"type": "abstract",
"text": [
"mirAct: a web tool for evaluating microRNA activity based on gene expression data.\nMicroRNAs (miRNAs) are critical regulators in the complex cellular networks. The mirAct web server (http://sysbio.ustc.edu.cn/software/mirAct) is a tool designed to investigate miRNA activity based on gene-expression data by using the negative regulation relationship between miRNAs and their target genes. mirAct supports multiple-class data and enables clustering analysis based on computationally determined miRNA activity. Here, we describe the framework of mirAct, demonstrate its performance by comparing with other similar programs and exemplify its applications using case studies.\n"
],
"offsets": [
[
0,
673
]
]
}
] | [
{
"id": "PMID-21596785_T1",
"type": "Cell",
"text": [
"cellular"
],
"offsets": [
[
141,
149
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-10823148 | PMID-10823148 | [
{
"id": "PMID-10823148__text",
"type": "abstract",
"text": [
"Application of microsatellite PCR techniques in the identification of mixed up tissue specimens in surgical pathology.\nA fragment of tumour was erroneously mixed up with an endometrial biopsy. Micro-satellite polymerase chain reaction (PCR) clearly demonstrated the extraneous nature of the fragment. Micro-satellite PCR may be useful for the identification of mis-labelled or mismatched tissue fragments in surgical pathology specimens.\n"
],
"offsets": [
[
0,
438
]
]
}
] | [
{
"id": "PMID-10823148_T1",
"type": "Tissue",
"text": [
"tissue specimens"
],
"offsets": [
[
79,
95
]
],
"normalized": []
},
{
"id": "PMID-10823148_T2",
"type": "Pathological_formation",
"text": [
"tumour"
],
"offsets": [
[
133,
139
]
],
"normalized": []
},
{
"id": "PMID-10823148_T3",
"type": "Tissue",
"text": [
"tissue fragments"
],
"offsets": [
[
388,
404
]
],
"normalized": []
},
{
"id": "PMID-10823148_T4",
"type": "Tissue",
"text": [
"specimens"
],
"offsets": [
[
427,
436
]
],
"normalized": []
},
{
"id": "PMID-10823148_T5",
"type": "Tissue",
"text": [
"endometrial biopsy"
],
"offsets": [
[
173,
191
]
],
"normalized": []
},
{
"id": "PMID-10823148_T6",
"type": "Pathological_formation",
"text": [
"fragment"
],
"offsets": [
[
121,
129
]
],
"normalized": []
},
{
"id": "PMID-10823148_T7",
"type": "Pathological_formation",
"text": [
"fragment"
],
"offsets": [
[
291,
299
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-10823148_R1",
"type": "Part-of",
"arg1_id": "PMID-10823148_T6",
"arg2_id": "PMID-10823148_T2",
"normalized": []
}
] |
PMC-3256136-sec-15 | PMC-3256136-sec-15 | [
{
"id": "PMC-3256136-sec-15__text",
"type": "sec",
"text": [
"Discussion\nWe estimated the future acceptability of PrEP, examining the attitudes and preferences of potential user groups from different countries towards hypothetical and known PrEP attributes. Our results show that participants were generally willing to accept PrEP and adopt it as soon as it becomes available. Surprisingly, participants were also willing to take PrEP even when reminded of potential side effects, cost, condom use, and frequent HIV testing. These findings indicate participants' motivation to overcome barriers which can have a considerable impact on uptake. In contrast, participants mentioned that the thought of taking PrEP made them feel anxious, although they also indicated that taking PrEP would not be embarrassing and they would want their partner or partners to know. Participants' anxiety may be explained by the hypothetical nature of most of the presented PrEP characteristics, the stigma associated with HIV [34], and in some settings, the criminalization of sex work, injected drug use and homosexuality [35]. Most participants, nonetheless, subsequently indicated that PrEP would give them hope, which suggests that their initial willingness to take it remained largely unscathed.\nFemale participants indicated a higher level of willingness to take PrEP than male participants, which may be explained by women's difficulty negotiating the use of condoms and awareness of their and/or their partners' risk of becoming infected with HIV [36]. We also found that younger participants and those with fewer children, those who reported adherence to past medication, more frequent condom usage, having been tested for HIV in the past and never injecting drugs, reported greater willingness to take PrEP. These promising findings suggest that those who are currently bearing the brunt of HIV [1], have higher perceived risk, and are most likely to adhere to a comprehensive PrEP program, are also the most motivated to enroll. Yet, while participants stated not being interested in selling PrEP, the majority reported intentions to share it. Therefore, information and counseling about the risks of sharing PrEP should be readily available as part of any implementation program.\nResults from the conjoint analysis reveal trends in participants' preferences which deserve consideration. PrEP route of administration was the most important attribute, and bi-monthly and monthly injections were the preferred alternatives. This finding is encouraging from a policy perspective if such modalities become available; since it may reduce users' likelihood of sharing, selling or forgetting to take PrEP, but it also raises questions regarding participants' willingness to take oral PrEP. HIV testing was the second most important attribute, and a test every six months was, as expected, the preferred alternative. Interestingly, dispensing sites were more important than any other attribute for some groups, particularly in Africa. This may indicate concerns about social stigma and access [37]. However, it is encouraging that most participants were willing to receive PrEP at a healthcare facility, which can facilitate synergies between PrEP and other existing prevention services. Time spent obtaining PrEP and frequency of pick up, which we used as a proxy measure for cost-opportunity, were generally less important, consistent with participants' willingness to pay for PrEP.\nOur findings are broadly consistent with the work of Guest et al. and Galea et al [18], [19]. However, specific comparisons are not advisable as the composition and size of the samples, recruitment methods, measures and statistical analyses differ greatly. Previous work on PrEP implementation suggests that delivery programs will need to meet a number of requirements in order to be effective, including: prioritization of groups at higher risk of infection; delivery of PrEP in combination with other prevention services, including risk reduction and medication adherence counseling, condoms provision, diagnosis and treatment of other sexually transmitted infections, and frequent HIV testing; and monitoring of side effects, adherence and risk behaviors [8], [38], [39], [40], [41], [42]. Our results provide valuable clues that can help countries to deliver PrEP more effectively, should they decide to implement it, by focusing their efforts on the aspects that need more attention.\nThis is the first multinational study, to our knowledge, that integrates different disciplines to shed light on a question that we believe is of global importance. Our study complements previous work on PrEP by examining potential users' perspective and offering insights into their attitudes and preferences. We note that it may not be possible to generalize the observed PrEP acceptability to other settings and our results should be considered within the context of this study's limitations. Given the sensitive nature of the addressed questions, and despite all our efforts to reduce social desirability bias, there is an unavoidable risk that participants may have felt at times compelled to provide what they felt was the \"right\" answer. Additionally, our data collection took place in urban areas, where HIV incidence is normally higher, thus current findings may not be generalizable to rural settings. Finally, examining acceptability among users enrolled in pilot programs is much deserving, as actual acceptability may differ from potential willingness to take PrEP, especially if relevant attributes of a product or program are modified, as observed in other comparable interventions [43].\n\n"
],
"offsets": [
[
0,
5598
]
]
}
] | [] | [] | [] | [] |
PMC-3041925-caption-05 | PMC-3041925-caption-05 | [
{
"id": "PMC-3041925-caption-05__text",
"type": "caption",
"text": [
"Intact mass analysis of a mixed population of proteins. A mixture of the membrane protein KCNJ12, the soluble TEV protease used to cleave the fusion tag, and the membrane protein HVCN1, which occurred as a contaminant from an earlier analysis on the same LC column.\n"
],
"offsets": [
[
0,
266
]
]
}
] | [
{
"id": "PMC-3041925-caption-05_T1",
"type": "Cellular_component",
"text": [
"membrane"
],
"offsets": [
[
73,
81
]
],
"normalized": []
},
{
"id": "PMC-3041925-caption-05_T2",
"type": "Cellular_component",
"text": [
"membrane"
],
"offsets": [
[
162,
170
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16101297 | PMID-16101297 | [
{
"id": "PMID-16101297__text",
"type": "abstract",
"text": [
"A novel conotoxin from Conus delessertii with posttranslationally modified lysine residues.\nA major peptide, de13a from the crude venom of Conus delessertii collected in the Yucatan Channel, Mexico, was purified. The peptide had a high content of posttranslationally modified amino acids, including 6-bromotryptophan and a nonstandard amino acid that proved to be 5-hydroxylysine. This is the first report of 5-hydroxylysine residues in conotoxins. The sequence analysis, together with cDNA cloning and a mass determination (monoisotopic mass of 3486.76 Da), established that the mature toxin has the sequence DCOTSCOTTCANGWECCKGYOCVNKACSGCTH, where O is 4-hydroxyproline, W 6-bromotryptophan, and K 5-hydroxylysine, the asterisk represents the amidated C-terminus, and the calculated monoisotopic mass is 3487.09 Da. The eight Cys residues are arranged in a pattern (C-C-C-CC-C-C-C) not described previously in conotoxins. This arrangement, for which we propose the designation of framework #13 or XIII, differs from the ones (C-C-CC-CC-C-C and C-C-C-C-CC-C-C) present in other conotoxins which also contain eight Cys residues. This peptide thus defines a novel class of conotoxins, with a new posttranslational modification not previously found in other Conus peptide families.\n"
],
"offsets": [
[
0,
1280
]
]
}
] | [
{
"id": "PMID-16101297_T1",
"type": "Organism_substance",
"text": [
"venom"
],
"offsets": [
[
130,
135
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-7828172 | PMID-7828172 | [
{
"id": "PMID-7828172__text",
"type": "abstract",
"text": [
"Differential effects of carbachol on calcium entry and release in CHO cells expressing the m3 muscarinic receptor.\nCalcium signalling was examined in CHO-k1 cells that stably express the m3 subtype of the muscarinic receptor. The calcium indicator Fura-2 was retained in these cells only in the presence of probenecid (1 mM), suggesting that Fura-2 efflux was mediated by an organic anion transporter. The addition of carbachol (CCh) to Fura-2 loaded cells in suspension caused a rapid transient increase in intracellular calcium [Ca]i followed by a smaller sustained plateau phase. The transient rise in [Ca]i was dose-dependent with a threshold response of 89 +/- 18 nM above baseline with 10 nM CCh and a maximum stimulation of 734 +/- 46 nM with 10 microM CCh. This phase was accompanied by a similar dose-dependent stimulation of total inositol phosphate production and was assumed to be generated by release from intracellular stores of the endoplasmic reticulum (ER). The sustained increase in [Ca]i was generated by entry from the extracellular bath since it was blocked by pretreatment with La3+ (1 microM) and was absent when bath calcium was chelated with EGTA. This phase was not dependent on CCh dose, and a stimulation of [Ca]i of approximately 90 nM above baseline was observed with CCh concentrations between 50 nM and 10 microM. With this dose range, the rate of Mn2+ quenching of Fura-2 at the Ca-insensitive excitation wavelength of 360 nm was likewise maximally stimulated. At lower CCh concentrations (10-50 nM), it was clear that the activation of Ca entry could not be dissociated from a threshold release of Ca from intracellular stores. The phorbol ester PMA, which uncouples the muscarinic receptor from phospholipase C, reduced the transient rise in [Ca]i by approximately 50% with little or no effect on Ca entry at higher CCh levels (> or = 1 microM). At lower CCh concentrations (< or = 100 nM) however, pretreatment with PMA completely blocked all Ca mobilization and supports the contention that Ca entry is coupled to Ca release from stores or to store depletion. The emptying of inositol trisphosphate-sensitive stores with thapsigargin (10 nM) stimulated Ca entry and also the rate of Mn2+ quenching. Store depletion by incubation in Ca-free media likewise stimulated Mn2+ uptake without a rise in [Ca]i. Our data are therefore consistent with a 'capacitative' coupling model, whereby the activation of the plasma membrane receptor leads to an InsP3-induced change in the degree of filling of the ER Ca pool.(ABSTRACT TRUNCATED AT 400 WORDS)\n"
],
"offsets": [
[
0,
2577
]
]
}
] | [
{
"id": "PMID-7828172_T1",
"type": "Cell",
"text": [
"CHO cells"
],
"offsets": [
[
66,
75
]
],
"normalized": []
},
{
"id": "PMID-7828172_T2",
"type": "Cell",
"text": [
"CHO-k1 cells"
],
"offsets": [
[
150,
162
]
],
"normalized": []
},
{
"id": "PMID-7828172_T3",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
277,
282
]
],
"normalized": []
},
{
"id": "PMID-7828172_T4",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
451,
456
]
],
"normalized": []
},
{
"id": "PMID-7828172_T7",
"type": "Cellular_component",
"text": [
"endoplasmic reticulum"
],
"offsets": [
[
947,
968
]
],
"normalized": []
},
{
"id": "PMID-7828172_T8",
"type": "Cellular_component",
"text": [
"ER"
],
"offsets": [
[
970,
972
]
],
"normalized": []
},
{
"id": "PMID-7828172_T9",
"type": "Immaterial_anatomical_entity",
"text": [
"extracellular"
],
"offsets": [
[
1039,
1052
]
],
"normalized": []
},
{
"id": "PMID-7828172_T10",
"type": "Cellular_component",
"text": [
"plasma membrane"
],
"offsets": [
[
2442,
2457
]
],
"normalized": []
},
{
"id": "PMID-7828172_T5",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
508,
521
]
],
"normalized": []
},
{
"id": "PMID-7828172_T6",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
919,
932
]
],
"normalized": []
},
{
"id": "PMID-7828172_T11",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1640,
1653
]
],
"normalized": []
},
{
"id": "PMID-7828172_T12",
"type": "Cellular_component",
"text": [
"ER"
],
"offsets": [
[
2532,
2534
]
],
"normalized": []
}
] | [] | [
{
"id": "PMID-7828172_1",
"entity_ids": [
"PMID-7828172_T7",
"PMID-7828172_T8"
]
}
] | [] |
PMID-15202612 | PMID-15202612 | [
{
"id": "PMID-15202612__text",
"type": "abstract",
"text": [
"Novel insights into the pathogenesis of uric acid nephrolithiasis.\nPURPOSE OF REVIEW:\nThe factors involved in the pathogenesis of uric acid nephrolithiasis are well known. A low urinary pH is the most significant element in the generation of stones, with hyperuricosuria being a less common finding. The underlying mechanism(s) responsible for these disturbances remain poorly characterized. This review summarizes previous knowledge and highlights some recent developments in the pathophysiology of low urine pH and hyperuricosuria.\nRECENT FINDINGS:\nEpidemiological and metabolic studies have indicated an association between uric acid nephrolithiasis and insulin resistance. Some potential mechanisms include impaired ammoniagenesis caused by resistance to insulin action in the renal proximal tubule, or substrate competition by free fatty acids. The evaluation of a large Sicilian kindred recently revealed a putative genetic locus linked to uric acid stone disease. The identification of novel complementary DNA has provided an interesting insight into the renal handling of uric acid, including one genetic cause of renal uric acid wasting.\nSUMMARY:\nThe recognition of metabolic, molecular, and genetic factors that influence urinary pH, and uric acid metabolism and excretion, will provide novel insights into the pathogenesis of uric acid stones, and open the way for new therapeutic strategies.\n"
],
"offsets": [
[
0,
1404
]
]
}
] | [
{
"id": "PMID-15202612_T1",
"type": "Organism_substance",
"text": [
"urinary"
],
"offsets": [
[
178,
185
]
],
"normalized": []
},
{
"id": "PMID-15202612_T2",
"type": "Organism_substance",
"text": [
"urine"
],
"offsets": [
[
504,
509
]
],
"normalized": []
},
{
"id": "PMID-15202612_T3",
"type": "Organ",
"text": [
"renal"
],
"offsets": [
[
1062,
1067
]
],
"normalized": []
},
{
"id": "PMID-15202612_T4",
"type": "Organ",
"text": [
"renal"
],
"offsets": [
[
1122,
1127
]
],
"normalized": []
},
{
"id": "PMID-15202612_T5",
"type": "Organism_substance",
"text": [
"urinary"
],
"offsets": [
[
1232,
1239
]
],
"normalized": []
},
{
"id": "PMID-15202612_T6",
"type": "Multi-tissue_structure",
"text": [
"renal proximal tubule"
],
"offsets": [
[
781,
802
]
],
"normalized": []
},
{
"id": "PMID-15202612_T7",
"type": "Organism_substance",
"text": [
"uric acid stone"
],
"offsets": [
[
946,
961
]
],
"normalized": []
},
{
"id": "PMID-15202612_T8",
"type": "Organism_substance",
"text": [
"stones"
],
"offsets": [
[
242,
248
]
],
"normalized": []
},
{
"id": "PMID-15202612_T9",
"type": "Organism_substance",
"text": [
"uric acid stones"
],
"offsets": [
[
1337,
1353
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-12884381 | PMID-12884381 | [
{
"id": "PMID-12884381__text",
"type": "abstract",
"text": [
"Stereoselective synthesis of 1-aminoalkanephosphonic acids with two chiral centers and their activity towards leucine aminopeptidase.\nThe stereoselective synthesis of 1-amino-2-alkylalkanephosphonic acids, namely, compounds bearing two chiral centers, was achieved by the condensation of hypophosphorous acid salts of (R)(+) or (S)(-)-N-alpha-methylbenzylamine with the appropriate aldehydes in isopropanol. Simultaneous deprotection and oxidation by the action of bromine water provided equimolar mixtures of the RS:RR and SR:SS diastereomers of desired acids. They appeared to act as moderate inhibitors of kidney leucine aminopeptidase with potency dependent on the absolute configuration of both centers of chirality.\n"
],
"offsets": [
[
0,
722
]
]
}
] | [
{
"id": "PMID-12884381_T1",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
609,
615
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3012732-sec-15 | PMC-3012732-sec-15 | [
{
"id": "PMC-3012732-sec-15__text",
"type": "sec",
"text": [
"Reagents and antibodies\nMaxisorp strips (NunC, Roskilde, Denmark), GST-PNMA2 recombinant protein (Abnova, Taipei, Taiwan); 3,3',5,5-tetramethylbenzidine (TMB) + substrate (Dako, Glostrup, Denmark), Peroxidase with dakocytomation peroxidase block (Dako), Dakocytomation envision(R) system labeled polymer-HRP anti-rabbit kit and 3-3'-diaminobenzidine (Dako), Mayer's hematoxylin (Histolab Product AB, Gothenburg, Sweden), Graded alcohol (Kemetyl, Vestby, Norway), Xylen (Solveco, Rosersberg, Sweden), Pertex(R) (Histolab, Gothenburg, Sweden), Tris-Glycine blotting buffer (Amresco, Solon, OH), Western blotting (WB) reagent and Lumi-Light WB substrate (Roche, Basel, Switzerland), EasyTag Methionine-L-35S, NEG709A005MC (PerkinElmer, Waltham, MA), Full-length cDNA clone for human PNMA2, ID6580976 (BioScience Geneservice, Cambridge, UK), TnT(R) SP6 Quick Coupled Transcription/Translation System (Promega, Madison, WI), Protein G-Sepharose beads (GE Healthcare, Little Chalfont, Buckinghamshire, UK), Peroxidase (HRP)-conjugated rabbit anti human IgG (anti-IgG) (Dako), rabbit polyclonal antibody anti-PNMA2 (Atlas Antibodies, Stockholm, Sweden), monoclonal mouse anti-GST, sc-138, polyclonal goat anti-human Ma2, sc-68099, HRP-donkey anti-goat, sc-2020, (Santa Cruz Biotechnology, Santa Cruz, CA), HRP-goat anti-rabbit, P0448, (Dako) and Ravo PNS-Blot, (Ravo Diagnostika GmbH, Freiburg, Germany).\n"
],
"offsets": [
[
0,
1398
]
]
}
] | [] | [] | [] | [] |
PMID-6920468 | PMID-6920468 | [
{
"id": "PMID-6920468__text",
"type": "abstract",
"text": [
"Relationship of self-concept during late pregnancy to neonatal perception and parenting profile.\nThirty-one gravidas were studied to examine the relationship between a woman's feelings about herself during late pregnancy, her perception of her newborn, and her profile of parenting. The Tennessee Self-Concept Scale was completed during the third trimester of pregnancy, the Neonatal Perception Inventory I at one-to-two days postpartum, and the Neonatal Perception Inventory II and the Michigan Screening Profile of Parenting at four-to-six weeks postpartum. When considered separately, no positive significant relationships were found between scores on these variables. However, all subjects with negative scores on both self-concept and neonatal perception had negative scores on at least two subscales of the parenting profile.\n"
],
"offsets": [
[
0,
832
]
]
}
] | [] | [] | [] | [] |
PMC-3052613-caption-01 | PMC-3052613-caption-01 | [
{
"id": "PMC-3052613-caption-01__text",
"type": "caption",
"text": [
"Modified radiology-guided percutaneous gastrostomy technique.\nA. 21G fine needle punctured localized collection of air, which was visible in collapsed stomach under fluoroscopy-guided gastrostomy. Needle tip is then gradually withdrawn while injecting small amounts of water-soluble contrast medium. Location of stomach is confirmed by visualization of opacified gastric rugae. B. Stomach was inflated with approximately 600-800 mL of room air through 21G fine needle. C. 100-cm stainless steel guide wire is inserted through needle, and gastro-percutaneous tract is gradually dilated. D. Insertion of 14-Fr pigtail gastrostomy catheter and injection of small amount of water-soluble contrast medium via pigtail catheter confirmed that gastrostomy catheter is correctly placed within stomach.\n"
],
"offsets": [
[
0,
793
]
]
}
] | [
{
"id": "PMC-3052613-caption-01_T1",
"type": "Organ",
"text": [
"stomach"
],
"offsets": [
[
151,
158
]
],
"normalized": []
},
{
"id": "PMC-3052613-caption-01_T2",
"type": "Organ",
"text": [
"stomach"
],
"offsets": [
[
312,
319
]
],
"normalized": []
},
{
"id": "PMC-3052613-caption-01_T3",
"type": "Organ",
"text": [
"gastric"
],
"offsets": [
[
363,
370
]
],
"normalized": []
},
{
"id": "PMC-3052613-caption-01_T4",
"type": "Organ",
"text": [
"Stomach"
],
"offsets": [
[
381,
388
]
],
"normalized": []
},
{
"id": "PMC-3052613-caption-01_T5",
"type": "Organ",
"text": [
"gastro"
],
"offsets": [
[
538,
544
]
],
"normalized": []
},
{
"id": "PMC-3052613-caption-01_T6",
"type": "Organ",
"text": [
"stomach"
],
"offsets": [
[
784,
791
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-10080451 | PMID-10080451 | [
{
"id": "PMID-10080451__text",
"type": "abstract",
"text": [
"Ventricular fibrillation due to long QT syndrome probably caused by clindamycin.\nProlongation of QT time interval may be provoked by a limited number of drugs, especially macrolide antibiotics. We describe a case of QT time interval prolongation induced by clindamycin with subsequent repeated ventricular fibrillation and resuscitation; there is no previous report in the literature of QT time prolongation caused by lincosamides.\n"
],
"offsets": [
[
0,
432
]
]
}
] | [
{
"id": "PMID-10080451_T1",
"type": "Multi-tissue_structure",
"text": [
"Ventricular"
],
"offsets": [
[
0,
11
]
],
"normalized": []
},
{
"id": "PMID-10080451_T2",
"type": "Multi-tissue_structure",
"text": [
"ventricular"
],
"offsets": [
[
294,
305
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-19752254 | PMID-19752254 | [
{
"id": "PMID-19752254__text",
"type": "abstract",
"text": [
"Magnesium for treatment of asthma in children.\nQUESTION: Magnesium is considered adjuvant therapy for moderate to severe asthma exacerbations in adults, but can it be used to treat children? ANSWER: Magnesium seems to be beneficial in the treatment of moderate to severe asthma in children. It is a safe drug to administer, but there have been minor side effects reported, such as epigastric or facial warmth, flushing, pain and numbness at the infusion site, dry mouth, malaise, and hypotension. Owing to its bronchodilating and anti-inflammatory effects, magnesium is an encouraging adjuvant therapy for pediatric patients who do not respond to conventional treatment in acute severe exacerbations. Future studies should focus on establishing the optimal dosage for maximal benefits and the best route of administration. Magnesium should also be considered as a prophylactic treatment.\n"
],
"offsets": [
[
0,
888
]
]
}
] | [
{
"id": "PMID-19752254_T1",
"type": "Organism_subdivision",
"text": [
"epigastric"
],
"offsets": [
[
381,
391
]
],
"normalized": []
},
{
"id": "PMID-19752254_T2",
"type": "Organism_subdivision",
"text": [
"facial"
],
"offsets": [
[
395,
401
]
],
"normalized": []
},
{
"id": "PMID-19752254_T3",
"type": "Organism_subdivision",
"text": [
"mouth"
],
"offsets": [
[
464,
469
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3168770-caption-05 | PMC-3168770-caption-05 | [
{
"id": "PMC-3168770-caption-05__text",
"type": "caption",
"text": [
"Challenges to creating and implementing a perioperative glycemic control protocol.\n"
],
"offsets": [
[
0,
83
]
]
}
] | [] | [] | [] | [] |
PMC-2769146-sec-05 | PMC-2769146-sec-05 | [
{
"id": "PMC-2769146-sec-05__text",
"type": "sec",
"text": [
"3.2.\nCell line and culture\nDU145 (prostate cancer) cell line was used in this assay. DU145 was grown in DMEM/F-12 medium (Gibco BRL Life Technologies, San Diego, CA., USA) supplemented with 10% fetal calf serum and kept in a humidified 37 degreesC, 5% CO2 incubator.\n"
],
"offsets": [
[
0,
267
]
]
}
] | [
{
"id": "PMC-2769146-sec-05_T1",
"type": "Cell",
"text": [
"Cell line"
],
"offsets": [
[
5,
14
]
],
"normalized": []
},
{
"id": "PMC-2769146-sec-05_T2",
"type": "Cell",
"text": [
"DU145 (prostate cancer) cell line"
],
"offsets": [
[
27,
60
]
],
"normalized": []
},
{
"id": "PMC-2769146-sec-05_T3",
"type": "Cell",
"text": [
"DU145"
],
"offsets": [
[
85,
90
]
],
"normalized": []
},
{
"id": "PMC-2769146-sec-05_T4",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
205,
210
]
],
"normalized": []
},
{
"id": "PMC-2769146-sec-05_T5",
"type": "Developing_anatomical_structure",
"text": [
"fetal"
],
"offsets": [
[
194,
199
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-2607031 | PMID-2607031 | [
{
"id": "PMID-2607031__text",
"type": "abstract",
"text": [
"Screening method for insecticidal activity using first instars of black blow fly (Diptera: Calliphoridae).\nA bioassay method suitable for rapid mass screening of fermentation and synthetic organic compounds for insecticidal activity is described. The test, which uses first instars of susceptible black blow fly, Phormia regina (Meigen), in a bovine serum medium, detects insecticidal activity with reproducible results. It is capable of selecting the most active compound in structure-activity relationships by minimum effective dose concentration studies. The bioassay system is easy to operate and requires only a minute quantity of chemical compound.\n"
],
"offsets": [
[
0,
655
]
]
}
] | [
{
"id": "PMID-2607031_T1",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
350,
355
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-9671543 | PMID-9671543 | [
{
"id": "PMID-9671543__text",
"type": "abstract",
"text": [
"Acylase I-catalyzed deacetylation of N-acetyl-L-cysteine and S-alkyl-N-acetyl-L-cysteines.\nThe aminoacylase that catalyzes the hydrolysis of N-acetyl-L-cysteine (NAC) was identified as acylase I after purification by column chromatography and electrophoretic analysis. Rat kidney cytosol was fractionated by ammonium sulfate precipitation, and the proteins were separated by ion-exchange column chromatography, gel-filtration column chromatography, and hydrophobic interaction column chromatography. Acylase activity with NAC and N-acetyl-L-methionine (NAM), a known substrate for acylase I, as substrates coeluted during all chromatographic steps. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that the protein was purified to near homogeneity and had a subunit Mr of 43 000, which is identical with the Mr of acylase I from porcine kidney and bovine liver. n-Butylmalonic acid was a slow-binding inhibitor of acylase I and inhibited the deacetylation of NAC with a Ki of 192 +/- 27 microM. These results show that acylase I catalyzes the deacetylation of NAC. The acylase I-catalyzed deacetylation of a range of S-alkyl-N-acetyl-L-cysteines, their carbon and oxygen analogues, and the selenium analogue of NAM was also studied with porcine kidney acylase I. The specific activity of the acylase I-catalyzed deacetylation of these substrates was related to their calculated molar volumes and log P values. The S-alkyl-N-acetyl-L-cysteines with short (C0-C3) and unbranched S-alkyl substituents were good acylase I substrates, whereas the S-alkyl-N-acetyl-L-cysteines with long (>C3) and branched S-alkyl substituents were poLr acylase I substrates. The carbon and oxygen analogues of S-methyl-N-acetyl-L-cysteine and the carbon analogue of S-ethyl-N-acetyl-L-cysteine were poor acylase I substrates, whereas the selenium analogue of NAM was a good acylase I substrate.\n"
],
"offsets": [
[
0,
1889
]
]
}
] | [
{
"id": "PMID-9671543_T1",
"type": "Organism_substance",
"text": [
"kidney cytosol"
],
"offsets": [
[
273,
287
]
],
"normalized": []
},
{
"id": "PMID-9671543_T2",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
853,
859
]
],
"normalized": []
},
{
"id": "PMID-9671543_T3",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
871,
876
]
],
"normalized": []
},
{
"id": "PMID-9671543_T4",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
1261,
1267
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16773443 | PMID-16773443 | [
{
"id": "PMID-16773443__text",
"type": "abstract",
"text": [
"Fluoro-Jade B staining following zymosan microinjection into the spinal cord white matter.\n1. The fluorescein derivate Fluoro-Jade B (FJB), which primarily labels dead or dying neurons, was used to study the acute focal inflammation in the spinal cord white matter. Inflammation was induced by microinjection of the yeast particulate zymosan to evaluate the biological effects of intraspinal macrophages activation without the confounding effects of physical trauma. 2. A single bolus of zymosan (Sigma, 75 nL) was stereotaxically injected at the thoracic level into the lateral white matter of rat spinal cord. A standard Fluoro-Jade B staining protocol was applied to spinal cord sections at 6, 12, 24 h and 2, 4 days postinjection. Neutral Red, NADPH-diaphorase, Iba1-IR, and DAPI staining protocols accomplished examination of the cells participating in the acute inflammatory response. 3. Zymosan caused formation of clearly delineated inflammation lesions localized in the lateral white matter of the spinal cord. Fluoro-Jade B stained cells in the area of inflammation were not observed at 12 h postinjection while mild FJB staining appeared at 24 h and intense staining was observed at 2 and 4 days postinjection. 4. This study shows that the acute response to zymosan-induced inflammation in the rat spinal cord white matter causes a gradual appearance of phagocytic microglia/macrophages and delayed FJB staining of the inflammatory cells. 5. FJB, a reliable marker of dying neurons, is a more universal agent than formerly believed. One possible explanation for the gradual appearance of FJB-stained cells in the area of inflammation is that specific time is required for sufficient levels of proteins and/or myelin debris of axonal origin to appear in the cytoplasm of phagocytic microglia/macrophages.\n"
],
"offsets": [
[
0,
1815
]
]
}
] | [
{
"id": "PMID-16773443_T1",
"type": "Multi-tissue_structure",
"text": [
"spinal cord white matter"
],
"offsets": [
[
65,
89
]
],
"normalized": []
},
{
"id": "PMID-16773443_T2",
"type": "Cell",
"text": [
"neurons"
],
"offsets": [
[
177,
184
]
],
"normalized": []
},
{
"id": "PMID-16773443_T3",
"type": "Multi-tissue_structure",
"text": [
"spinal cord white matter"
],
"offsets": [
[
240,
264
]
],
"normalized": []
},
{
"id": "PMID-16773443_T4",
"type": "Multi-tissue_structure",
"text": [
"lateral white matter"
],
"offsets": [
[
571,
591
]
],
"normalized": []
},
{
"id": "PMID-16773443_T5",
"type": "Organ",
"text": [
"spinal cord"
],
"offsets": [
[
599,
610
]
],
"normalized": []
},
{
"id": "PMID-16773443_T6",
"type": "Organ",
"text": [
"spinal cord"
],
"offsets": [
[
670,
681
]
],
"normalized": []
},
{
"id": "PMID-16773443_T7",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
835,
840
]
],
"normalized": []
},
{
"id": "PMID-16773443_T8",
"type": "Organ",
"text": [
"spinal cord"
],
"offsets": [
[
1007,
1018
]
],
"normalized": []
},
{
"id": "PMID-16773443_T9",
"type": "Multi-tissue_structure",
"text": [
"lateral white matter"
],
"offsets": [
[
979,
999
]
],
"normalized": []
},
{
"id": "PMID-16773443_T10",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
1042,
1047
]
],
"normalized": []
},
{
"id": "PMID-16773443_T11",
"type": "Multi-tissue_structure",
"text": [
"spinal cord white matter"
],
"offsets": [
[
1309,
1333
]
],
"normalized": []
},
{
"id": "PMID-16773443_T12",
"type": "Cell",
"text": [
"phagocytic microglia"
],
"offsets": [
[
1365,
1385
]
],
"normalized": []
},
{
"id": "PMID-16773443_T13",
"type": "Cell",
"text": [
"macrophages"
],
"offsets": [
[
1386,
1397
]
],
"normalized": []
},
{
"id": "PMID-16773443_T14",
"type": "Cell",
"text": [
"inflammatory cells"
],
"offsets": [
[
1430,
1448
]
],
"normalized": []
},
{
"id": "PMID-16773443_T15",
"type": "Cell",
"text": [
"neurons"
],
"offsets": [
[
1485,
1492
]
],
"normalized": []
},
{
"id": "PMID-16773443_T16",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
1611,
1616
]
],
"normalized": []
},
{
"id": "PMID-16773443_T17",
"type": "Pathological_formation",
"text": [
"inflammation lesions"
],
"offsets": [
[
941,
961
]
],
"normalized": []
},
{
"id": "PMID-16773443_T18",
"type": "Pathological_formation",
"text": [
"inflammation"
],
"offsets": [
[
1063,
1075
]
],
"normalized": []
},
{
"id": "PMID-16773443_T19",
"type": "Pathological_formation",
"text": [
"inflammation"
],
"offsets": [
[
1632,
1644
]
],
"normalized": []
},
{
"id": "PMID-16773443_T20",
"type": "Organism_substance",
"text": [
"cytoplasm"
],
"offsets": [
[
1768,
1777
]
],
"normalized": []
},
{
"id": "PMID-16773443_T21",
"type": "Cell",
"text": [
"phagocytic microglia"
],
"offsets": [
[
1781,
1801
]
],
"normalized": []
},
{
"id": "PMID-16773443_T22",
"type": "Cell",
"text": [
"macrophages"
],
"offsets": [
[
1802,
1813
]
],
"normalized": []
},
{
"id": "PMID-16773443_T24",
"type": "Cell",
"text": [
"intraspinal macrophages"
],
"offsets": [
[
380,
403
]
],
"normalized": []
},
{
"id": "PMID-16773443_T25",
"type": "Multi-tissue_structure",
"text": [
"thoracic"
],
"offsets": [
[
547,
555
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-16773443_R1",
"type": "Part-of",
"arg1_id": "PMID-16773443_T4",
"arg2_id": "PMID-16773443_T5",
"normalized": []
},
{
"id": "PMID-16773443_R2",
"type": "Part-of",
"arg1_id": "PMID-16773443_T9",
"arg2_id": "PMID-16773443_T8",
"normalized": []
},
{
"id": "PMID-16773443_R3",
"type": "Part-of",
"arg1_id": "PMID-16773443_T10",
"arg2_id": "PMID-16773443_T18",
"normalized": []
},
{
"id": "PMID-16773443_R4",
"type": "Part-of",
"arg1_id": "PMID-16773443_T16",
"arg2_id": "PMID-16773443_T19",
"normalized": []
},
{
"id": "PMID-16773443_R5",
"type": "Part-of",
"arg1_id": "PMID-16773443_T20",
"arg2_id": "PMID-16773443_T21",
"normalized": []
},
{
"id": "PMID-16773443_R6",
"type": "Part-of",
"arg1_id": "PMID-16773443_T20",
"arg2_id": "PMID-16773443_T22",
"normalized": []
}
] |
PMC-3245051-caption-01 | PMC-3245051-caption-01 | [
{
"id": "PMC-3245051-caption-01__text",
"type": "caption",
"text": [
"The growth in the number of database publications per year. Each bar shows the number of research articles with the keyword 'database' appearing in the article title in the given year. The count only covers articles indexed in PubMed. The increase shows an exponential trend that will produce nearly 2000 database publications per year by 2015.\n"
],
"offsets": [
[
0,
345
]
]
}
] | [] | [] | [] | [] |
PMID-2704697 | PMID-2704697 | [
{
"id": "PMID-2704697__text",
"type": "abstract",
"text": [
"Early post-mortem metabolism and muscle shortening in the Pectoralis major muscle of broiler chickens.\nThree experiments were conducted to examine the effects of sodium pentobarbital (SP), iodoacetate (IO), tubocurarine (TC), and surgical denervation (DN) on early rigor development in broiler breast muscle. In Experiment 1, birds were either anesthetized or not with SP before receiving an injection of IO or TC or maintained as noninjected controls. Experiment 2 was identical except that a treatment of denervation of the breast muscle was added. Experiment 3 was conducted to contrast birds at 1 day (DN1) and 3 days (DN3) denervation prior to slaughter to nonoperated controls. Measurements of muscle lactate, ATP, R value (ratio of inosine to adenine nucleotides), pH, sarcomere lengths, and shear were used to evaluate treatment effects. Results for Experiment 1 showed no significant differences among treatment and control groups for ATP and lactate contents, R values, or sarcomere lengths; however, significantly lower pH and higher shear values were observed for control birds. In Experiment 2, no significant differences were observed among the treatment groups for ATP, R values, or sarcomere lengths. However, lactate and shear values were significantly lower, and pH higher, for the DN and SP treated birds. Experiment 3 resulted in lower lactate and higher pH values for the DN3 treatment in comparison with both DN1 and control groups. Results of these studies indicate that the use of SP and DN can be used to alter the early profiles of rigor development.\n"
],
"offsets": [
[
0,
1577
]
]
}
] | [
{
"id": "PMID-2704697_T1",
"type": "Organ",
"text": [
"muscle"
],
"offsets": [
[
33,
39
]
],
"normalized": []
},
{
"id": "PMID-2704697_T2",
"type": "Organ",
"text": [
"muscle"
],
"offsets": [
[
75,
81
]
],
"normalized": []
},
{
"id": "PMID-2704697_T3",
"type": "Organ",
"text": [
"breast muscle"
],
"offsets": [
[
294,
307
]
],
"normalized": []
},
{
"id": "PMID-2704697_T4",
"type": "Organ",
"text": [
"breast muscle"
],
"offsets": [
[
526,
539
]
],
"normalized": []
},
{
"id": "PMID-2704697_T5",
"type": "Organ",
"text": [
"muscle"
],
"offsets": [
[
700,
706
]
],
"normalized": []
},
{
"id": "PMID-2704697_T6",
"type": "Tissue",
"text": [
"sarcomere"
],
"offsets": [
[
776,
785
]
],
"normalized": []
},
{
"id": "PMID-2704697_T7",
"type": "Tissue",
"text": [
"sarcomere"
],
"offsets": [
[
983,
992
]
],
"normalized": []
},
{
"id": "PMID-2704697_T8",
"type": "Tissue",
"text": [
"sarcomere"
],
"offsets": [
[
1198,
1207
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3087566-caption-11 | PMC-3087566-caption-11 | [
{
"id": "PMC-3087566-caption-11__text",
"type": "caption",
"text": [
"Representative time histories of the estimated SatO2 levels of normal cortex (black) and tumor (grey) from all six patients.\n"
],
"offsets": [
[
0,
125
]
]
}
] | [
{
"id": "PMC-3087566-caption-11_T1",
"type": "Multi-tissue_structure",
"text": [
"cortex"
],
"offsets": [
[
70,
76
]
],
"normalized": []
},
{
"id": "PMC-3087566-caption-11_T2",
"type": "Pathological_formation",
"text": [
"tumor"
],
"offsets": [
[
89,
94
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-17432972 | PMID-17432972 | [
{
"id": "PMID-17432972__text",
"type": "abstract",
"text": [
"The relationship between brain activity and peak grip force is modulated by corticospinal system integrity after subcortical stroke.\nIn healthy human subjects, the relative contribution of cortical regions to motor performance varies with the task parameters. Additionally, after stroke, recruitment of cortical areas during a simple motor task varies with corticospinal system integrity. We investigated whether the pattern of motor system recruitment in a task involving increasingly forceful hand grips is influenced by the degree of corticospinal system damage. Nine chronic subcortical stroke patients and nine age-matched controls underwent functional magnetic brain imaging whilst performing repetitive isometric hand grips. Target grip forces were varied between 15% and 45% of individual maximum grip force. Corticospinal system functional integrity was assessed with transcranial magnetic stimulation. Averaged across all forces, there was more task-related activation compared with rest in the secondary motor areas of patients with greater corticospinal system damage, confirming previous reports. However, here we were primarily interested in regional brain activation, which covaried with the amount of force generated, implying a prominent executive role in force production. We found that in control subjects and patients with lesser corticospinal system damage, signal change increased linearly with increasing force output in contralateral primary motor cortex, supplementary motor area and ipsilateral cerebellum. In contrast, in patients with greater corticospinal system damage, force-related signal changes were seen mainly in contralesional dorsolateral premotor cortex, bilateral ventrolateral premotor cortices and contralesional cerebellum, but not ipsilesional primary motor cortex. These findings suggest that the premotor cortices might play a new and functionally relevant role in controlling force production in patients with more severe corticospinal system disruption.\n"
],
"offsets": [
[
0,
2002
]
]
}
] | [
{
"id": "PMID-17432972_T1",
"type": "Organ",
"text": [
"brain"
],
"offsets": [
[
25,
30
]
],
"normalized": []
},
{
"id": "PMID-17432972_T2",
"type": "Multi-tissue_structure",
"text": [
"cortical regions"
],
"offsets": [
[
189,
205
]
],
"normalized": []
},
{
"id": "PMID-17432972_T3",
"type": "Multi-tissue_structure",
"text": [
"cortical areas"
],
"offsets": [
[
303,
317
]
],
"normalized": []
},
{
"id": "PMID-17432972_T4",
"type": "Organism_subdivision",
"text": [
"hand"
],
"offsets": [
[
495,
499
]
],
"normalized": []
},
{
"id": "PMID-17432972_T5",
"type": "Organ",
"text": [
"brain"
],
"offsets": [
[
667,
672
]
],
"normalized": []
},
{
"id": "PMID-17432972_T6",
"type": "Organism_subdivision",
"text": [
"hand"
],
"offsets": [
[
720,
724
]
],
"normalized": []
},
{
"id": "PMID-17432972_T7",
"type": "Organ",
"text": [
"brain"
],
"offsets": [
[
1165,
1170
]
],
"normalized": []
},
{
"id": "PMID-17432972_T8",
"type": "Multi-tissue_structure",
"text": [
"motor cortex"
],
"offsets": [
[
1466,
1478
]
],
"normalized": []
},
{
"id": "PMID-17432972_T9",
"type": "Multi-tissue_structure",
"text": [
"cerebellum"
],
"offsets": [
[
1521,
1531
]
],
"normalized": []
},
{
"id": "PMID-17432972_T10",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
1571,
1591
]
],
"normalized": []
},
{
"id": "PMID-17432972_T11",
"type": "Multi-tissue_structure",
"text": [
"contralesional dorsolateral premotor cortex"
],
"offsets": [
[
1649,
1692
]
],
"normalized": []
},
{
"id": "PMID-17432972_T12",
"type": "Multi-tissue_structure",
"text": [
"bilateral ventrolateral premotor cortices"
],
"offsets": [
[
1694,
1735
]
],
"normalized": []
},
{
"id": "PMID-17432972_T13",
"type": "Multi-tissue_structure",
"text": [
"contralesional cerebellum"
],
"offsets": [
[
1740,
1765
]
],
"normalized": []
},
{
"id": "PMID-17432972_T14",
"type": "Multi-tissue_structure",
"text": [
"ipsilesional primary motor cortex"
],
"offsets": [
[
1775,
1808
]
],
"normalized": []
},
{
"id": "PMID-17432972_T15",
"type": "Multi-tissue_structure",
"text": [
"premotor cortices"
],
"offsets": [
[
1842,
1859
]
],
"normalized": []
},
{
"id": "PMID-17432972_T16",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
1969,
1989
]
],
"normalized": []
},
{
"id": "PMID-17432972_T17",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
76,
96
]
],
"normalized": []
},
{
"id": "PMID-17432972_T18",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
357,
377
]
],
"normalized": []
},
{
"id": "PMID-17432972_T19",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
537,
557
]
],
"normalized": []
},
{
"id": "PMID-17432972_T20",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
1052,
1072
]
],
"normalized": []
},
{
"id": "PMID-17432972_T21",
"type": "Anatomical_system",
"text": [
"corticospinal system"
],
"offsets": [
[
1350,
1370
]
],
"normalized": []
},
{
"id": "PMID-17432972_T22",
"type": "Multi-tissue_structure",
"text": [
"subcortical"
],
"offsets": [
[
113,
124
]
],
"normalized": []
},
{
"id": "PMID-17432972_T23",
"type": "Multi-tissue_structure",
"text": [
"subcortical"
],
"offsets": [
[
579,
590
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-2331105 | PMID-2331105 | [
{
"id": "PMID-2331105__text",
"type": "abstract",
"text": [
"The enlarging clinical spectrum of Lyme disease: Lyme cerebral vasculitis, a new disease entity.\nThe case of a patient with cerebral vasculitis with a right thalamic infarct associated with cerebral spinal fluid Lyme disease is presented. This entity has not been described in the United States, and only one similar case in the world literature could be found. The patient presented with a progressive headache and subsequent development of grand mal seizure activity. Lyme disease has been associated with cranial nerve palsies, peripheral and cranial radiculopathies, aseptic meningitis, encephalitic symptoms, chorea, and demyelinating polyneuropathy presenting like Guillain-Barre syndrome. These syndromes can occur separately or in combination. Stroke and strokelike syndromes have been attributed to Lyme disease. The literature concerning the neurologic manifestations of Lyme disease is reviewed.\n"
],
"offsets": [
[
0,
907
]
]
}
] | [
{
"id": "PMID-2331105_T1",
"type": "Organ",
"text": [
"cerebral"
],
"offsets": [
[
54,
62
]
],
"normalized": []
},
{
"id": "PMID-2331105_T2",
"type": "Organ",
"text": [
"cerebral"
],
"offsets": [
[
124,
132
]
],
"normalized": []
},
{
"id": "PMID-2331105_T3",
"type": "Organism_substance",
"text": [
"cerebral spinal fluid"
],
"offsets": [
[
190,
211
]
],
"normalized": []
},
{
"id": "PMID-2331105_T4",
"type": "Multi-tissue_structure",
"text": [
"cranial nerve"
],
"offsets": [
[
508,
521
]
],
"normalized": []
},
{
"id": "PMID-2331105_T5",
"type": "Organism_subdivision",
"text": [
"cranial"
],
"offsets": [
[
546,
553
]
],
"normalized": []
},
{
"id": "PMID-2331105_T6",
"type": "Multi-tissue_structure",
"text": [
"right thalamic"
],
"offsets": [
[
151,
165
]
],
"normalized": []
},
{
"id": "PMID-2331105_T7",
"type": "Anatomical_system",
"text": [
"neurologic"
],
"offsets": [
[
852,
862
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2984323-caption-02 | PMC-2984323-caption-02 | [
{
"id": "PMC-2984323-caption-02__text",
"type": "caption",
"text": [
"Characteristics of fistula lesions\n"
],
"offsets": [
[
0,
35
]
]
}
] | [
{
"id": "PMC-2984323-caption-02_T1",
"type": "Pathological_formation",
"text": [
"fistula lesions"
],
"offsets": [
[
19,
34
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-3763732 | PMID-3763732 | [
{
"id": "PMID-3763732__text",
"type": "abstract",
"text": [
"Unsatisfactory forehead scar following face lift.\nThe W-plasty scar revision technique has been found to be effective in the repair of the difficult and cosmetically unsatisfactory hairline scar following the ill-advised face lift technique that excises forehead skin.\n"
],
"offsets": [
[
0,
269
]
]
}
] | [
{
"id": "PMID-3763732_T1",
"type": "Pathological_formation",
"text": [
"forehead scar"
],
"offsets": [
[
15,
28
]
],
"normalized": []
},
{
"id": "PMID-3763732_T2",
"type": "Organism_subdivision",
"text": [
"face"
],
"offsets": [
[
39,
43
]
],
"normalized": []
},
{
"id": "PMID-3763732_T3",
"type": "Pathological_formation",
"text": [
"scar"
],
"offsets": [
[
63,
67
]
],
"normalized": []
},
{
"id": "PMID-3763732_T4",
"type": "Pathological_formation",
"text": [
"hairline scar"
],
"offsets": [
[
181,
194
]
],
"normalized": []
},
{
"id": "PMID-3763732_T5",
"type": "Organism_subdivision",
"text": [
"face"
],
"offsets": [
[
221,
225
]
],
"normalized": []
},
{
"id": "PMID-3763732_T6",
"type": "Multi-tissue_structure",
"text": [
"forehead skin"
],
"offsets": [
[
254,
267
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3238981-sec-11 | PMC-3238981-sec-11 | [
{
"id": "PMC-3238981-sec-11__text",
"type": "sec",
"text": [
"Figures\nFig. 1.\nA view of (I) with displacement ellipsoids drawn at the 30% probability level.\nFig. 2.\nStereoview of the sheet formed by C--H...pi interactions. Hydrogen atoms not involved in the motifs are not included.\n"
],
"offsets": [
[
0,
221
]
]
}
] | [] | [] | [] | [] |
PMID-3134031 | PMID-3134031 | [
{
"id": "PMID-3134031__text",
"type": "abstract",
"text": [
"Differential secretion of proteins and glycoproteins by livers of immature and adult rats. Effect of antimicrotubule drugs.\nThis study was initiated to re-examine reported differences in the action of antimicrotubule agents on plasma protein secretion from livers of immature versus adult rats. The aim was (1) to determine the composition and to monitor the secretion of various plasma proteins and glycoproteins from liver slices labeled in vitro with specific amino acids and sugar residues, and (2) to correlate observed differences in secretion of these proteins with structural changes in the hepatocytes of the different aged animals. For the most part, slices of liver from fetal (term), neonatal (4- to 5 days old), and adult rats (70 days old) were incubated with radioactive amino acids or various tritiated sugars specific for N-linked core oligosaccharide and/or N-linked terminal oligosaccharide chains. Our findings indicate that liver slices of fetal and neonatal rats are efficient in synthesizing plasma proteins including fully glycosylated glycoproteins. The secretion of glycosylated and nonglycosylated proteins believed to be processed through Golgi complexes was inhibited to the same extent (approximately 70-80%) by antimicrotubule agents, regardless of the age of the host animal. However, other proteins and glycoproteins secreted by livers of immature rats were found to be relatively insensitive (i.e. inhibited to only 30-40%) to the action of various antimicrotubule drugs. The glycoproteins were found to lack N-linked terminal sugars (although the glycoproteins did contain N-linked core sugars), and it is likely that the drug-insensitive proteins bypassed critical glycosylating sites in the Golgi compartment prior to release. Overall, these findings support earlier data showing that antimicrotubule drugs have a special impact on Golgi-associated events in liver cells. To what extent these findings are related to the action of microtubules remains to be seen.\n"
],
"offsets": [
[
0,
2001
]
]
}
] | [
{
"id": "PMID-3134031_T1",
"type": "Organ",
"text": [
"livers"
],
"offsets": [
[
56,
62
]
],
"normalized": []
},
{
"id": "PMID-3134031_T2",
"type": "Cellular_component",
"text": [
"microtubule"
],
"offsets": [
[
105,
116
]
],
"normalized": []
},
{
"id": "PMID-3134031_T3",
"type": "Cellular_component",
"text": [
"microtubule"
],
"offsets": [
[
205,
216
]
],
"normalized": []
},
{
"id": "PMID-3134031_T4",
"type": "Organism_substance",
"text": [
"plasma"
],
"offsets": [
[
227,
233
]
],
"normalized": []
},
{
"id": "PMID-3134031_T5",
"type": "Organ",
"text": [
"livers"
],
"offsets": [
[
257,
263
]
],
"normalized": []
},
{
"id": "PMID-3134031_T6",
"type": "Organism_substance",
"text": [
"plasma"
],
"offsets": [
[
380,
386
]
],
"normalized": []
},
{
"id": "PMID-3134031_T7",
"type": "Multi-tissue_structure",
"text": [
"liver slices"
],
"offsets": [
[
419,
431
]
],
"normalized": []
},
{
"id": "PMID-3134031_T8",
"type": "Cell",
"text": [
"hepatocytes"
],
"offsets": [
[
599,
610
]
],
"normalized": []
},
{
"id": "PMID-3134031_T9",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
671,
676
]
],
"normalized": []
},
{
"id": "PMID-3134031_T10",
"type": "Multi-tissue_structure",
"text": [
"slices"
],
"offsets": [
[
661,
667
]
],
"normalized": []
},
{
"id": "PMID-3134031_T11",
"type": "Developing_anatomical_structure",
"text": [
"fetal"
],
"offsets": [
[
682,
687
]
],
"normalized": []
},
{
"id": "PMID-3134031_T12",
"type": "Multi-tissue_structure",
"text": [
"liver slices"
],
"offsets": [
[
945,
957
]
],
"normalized": []
},
{
"id": "PMID-3134031_T13",
"type": "Developing_anatomical_structure",
"text": [
"fetal"
],
"offsets": [
[
961,
966
]
],
"normalized": []
},
{
"id": "PMID-3134031_T14",
"type": "Organism_substance",
"text": [
"plasma"
],
"offsets": [
[
1015,
1021
]
],
"normalized": []
},
{
"id": "PMID-3134031_T15",
"type": "Cellular_component",
"text": [
"Golgi complexes"
],
"offsets": [
[
1167,
1182
]
],
"normalized": []
},
{
"id": "PMID-3134031_T16",
"type": "Cellular_component",
"text": [
"microtubule"
],
"offsets": [
[
1246,
1257
]
],
"normalized": []
},
{
"id": "PMID-3134031_T17",
"type": "Organ",
"text": [
"livers"
],
"offsets": [
[
1362,
1368
]
],
"normalized": []
},
{
"id": "PMID-3134031_T18",
"type": "Cellular_component",
"text": [
"microtubule"
],
"offsets": [
[
1487,
1498
]
],
"normalized": []
},
{
"id": "PMID-3134031_T19",
"type": "Cellular_component",
"text": [
"Golgi compartment"
],
"offsets": [
[
1728,
1745
]
],
"normalized": []
},
{
"id": "PMID-3134031_T20",
"type": "Cellular_component",
"text": [
"microtubule"
],
"offsets": [
[
1826,
1837
]
],
"normalized": []
},
{
"id": "PMID-3134031_T21",
"type": "Cellular_component",
"text": [
"Golgi"
],
"offsets": [
[
1869,
1874
]
],
"normalized": []
},
{
"id": "PMID-3134031_T22",
"type": "Cell",
"text": [
"liver cells"
],
"offsets": [
[
1896,
1907
]
],
"normalized": []
},
{
"id": "PMID-3134031_T23",
"type": "Cellular_component",
"text": [
"microtubules"
],
"offsets": [
[
1968,
1980
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-3134031_R1",
"type": "Part-of",
"arg1_id": "PMID-3134031_T10",
"arg2_id": "PMID-3134031_T9",
"normalized": []
},
{
"id": "PMID-3134031_R2",
"type": "Part-of",
"arg1_id": "PMID-3134031_T9",
"arg2_id": "PMID-3134031_T11",
"normalized": []
},
{
"id": "PMID-3134031_R3",
"type": "Part-of",
"arg1_id": "PMID-3134031_T12",
"arg2_id": "PMID-3134031_T13",
"normalized": []
}
] |
PMID-10295626 | PMID-10295626 | [
{
"id": "PMID-10295626__text",
"type": "abstract",
"text": [
"Decontamination of medical equipment--manufacturer's problems.\n1. Small items sent via the post present a much greater hidden hazard and a higher potential for catching people unawares. 2. Large items accompanied by a Decontamination Certificate need to be treated with caution because only those surfaces which are accessible will have been cleaned; as soon as engineers start dismantling equipment, areas which are still soiled become exposed. 3. Total co-operation between hospital staff and service engineers is necessary to resolve these problems-neither can work safely without the assistance of the other. 4. Many products in use in hospitals may be up to 20 years old and clearly were not designed to facilitate decontamination and therefore present far greater risk to all concerned. 5. For the future there a clearly a responsibility with manufacturers to give more thought to the design of their equipment so that decontamination can be achieved more effectively.\n"
],
"offsets": [
[
0,
975
]
]
}
] | [] | [] | [] | [] |
PMC-3158436-sec-06 | PMC-3158436-sec-06 | [
{
"id": "PMC-3158436-sec-06__text",
"type": "sec",
"text": [
"2.1.3\nPixel Classification\nThe feature vector of a grid, which consists of nine features, is normalized to [0, 1], and the position features are scaled by the weighting coefficient wpos. Then, taking the nine dimensional vector of each grid as the input of the classifier, the ROI and non-ROI background in ultrasonic breast tumor images can be distinguished.\nIn this section, the self-organizing feature map neural network (SOMNN) [25], proposed by Kohonen according to characteristics of the nervous system, is used for the classification of these grids to detect the ROI automatically. The SOM is trained by the unsupervised learning to produce a low-dimensional discretized representation of the input space of the training samples, and it uses a neighborhood function to preserve the topological properties of the input space, which makes it different from other artificial neural networks.\nIn this way, the SOM is able to classify the sub-blocks into n clusters only by the unsupervised learning. In our study, the output layer number n is set to 2 (ROI and non-ROI output) and the feature vector extracted from each grid is taken as the input. To map the sorted sub-blocks back to the size of the original ultrasonic images, the initial result of ROI detection can be represented by a binary image as shown in Fig. (2d), where white areas indicate the ROI candidates while black areas the non-ROIs.\n"
],
"offsets": [
[
0,
1406
]
]
}
] | [
{
"id": "PMC-3158436-sec-06_T1",
"type": "Pathological_formation",
"text": [
"breast tumor"
],
"offsets": [
[
318,
330
]
],
"normalized": []
},
{
"id": "PMC-3158436-sec-06_T3",
"type": "Anatomical_system",
"text": [
"nervous system"
],
"offsets": [
[
494,
508
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-6327760 | PMID-6327760 | [
{
"id": "PMID-6327760__text",
"type": "abstract",
"text": [
"Use of monoclonal antibodies to investigate a possible role of thyroglobulin in the pathogenesis of Graves' ophthalmopathy.\nOne possible mechanism for Graves' ophthalmopathy is that the progressive orbital inflammation is initiated by formation of thyroglobulin (Tg)-anti-Tg immune complexes at sites of Tg binding to extraocular muscle membranes. In this study monoclonal antibodies (MCAB) against human Tg were used as probes (1) to identify Tg in eye muscle membranes prepared from normal subjects and (2) to measure binding of human Tg and Tg-anti-Tg immune complexes to eye muscle membranes. Reactivity of anti-Tg MCAB with Tg, thyroid, and eye muscle membranes was determined by binding of [125I]anti-Tg monoclonal antibody, an enzyme-linked immunosorbent assay (ELISA), and the indirect immunofluorescence technique. Seven membrane fractions, prepared by differential sucrose gradient centrifugation, were used. Whereas [125I]anti-Tg MCAB bound to all thyroid membrane fractions tested, no [125I]anti-Tg bound to eye muscle membranes. Similarly, reactivity of anti-Tg MCAB with eye muscle membranes was not demonstrated in ELISA or immunofluorescence tests. Although Tg-anti-Tg immune complexes bound to thyroid membranes, such complexes did not bind to eye muscle membranes. Significant binding of [125I]human Tg to eye muscle or thyroid membranes was not demonstrated for any membrane preparation. On the other hand moderate, but significant, binding to skeletal muscle was shown. Similar results were found using an ELISA. Binding of [125I]anti-Tg-Tg complexes of [125I]Tg to thyroid and eye muscle membranes was not affected by the presence of normal human serum, phosphate ions, pH, or incubation temperature, conditions claimed by others to be critical for Tg and Tg-anti-Tg immune complex binding. Since Tg is not present in normal human eye muscle a major role of Tg, or Tg-anti-Tg immune complexes, in the pathogenesis of Graves' ophthalmopathy appears to have been excluded by these findings.\n"
],
"offsets": [
[
0,
2010
]
]
}
] | [
{
"id": "PMID-6327760_T1",
"type": "Immaterial_anatomical_entity",
"text": [
"orbital"
],
"offsets": [
[
198,
205
]
],
"normalized": []
},
{
"id": "PMID-6327760_T2",
"type": "Tissue",
"text": [
"extraocular muscle membranes"
],
"offsets": [
[
318,
346
]
],
"normalized": []
},
{
"id": "PMID-6327760_T3",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
450,
470
]
],
"normalized": []
},
{
"id": "PMID-6327760_T4",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
575,
595
]
],
"normalized": []
},
{
"id": "PMID-6327760_T5",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
646,
666
]
],
"normalized": []
},
{
"id": "PMID-6327760_T6",
"type": "Tissue",
"text": [
"membrane fractions"
],
"offsets": [
[
830,
848
]
],
"normalized": []
},
{
"id": "PMID-6327760_T7",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
1085,
1105
]
],
"normalized": []
},
{
"id": "PMID-6327760_T8",
"type": "Tissue",
"text": [
"thyroid membranes"
],
"offsets": [
[
1211,
1228
]
],
"normalized": []
},
{
"id": "PMID-6327760_T9",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
1261,
1281
]
],
"normalized": []
},
{
"id": "PMID-6327760_T10",
"type": "Tissue",
"text": [
"eye muscle"
],
"offsets": [
[
1324,
1334
]
],
"normalized": []
},
{
"id": "PMID-6327760_T11",
"type": "Tissue",
"text": [
"thyroid membranes"
],
"offsets": [
[
1338,
1355
]
],
"normalized": []
},
{
"id": "PMID-6327760_T12",
"type": "Tissue",
"text": [
"membrane preparation"
],
"offsets": [
[
1385,
1405
]
],
"normalized": []
},
{
"id": "PMID-6327760_T14",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
1020,
1040
]
],
"normalized": []
},
{
"id": "PMID-6327760_T15",
"type": "Organ",
"text": [
"skeletal muscle"
],
"offsets": [
[
1463,
1478
]
],
"normalized": []
},
{
"id": "PMID-6327760_T16",
"type": "Tissue",
"text": [
"eye muscle membranes"
],
"offsets": [
[
1598,
1618
]
],
"normalized": []
},
{
"id": "PMID-6327760_T17",
"type": "Tissue",
"text": [
"thyroid"
],
"offsets": [
[
1586,
1593
]
],
"normalized": []
},
{
"id": "PMID-6327760_T18",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
1668,
1673
]
],
"normalized": []
},
{
"id": "PMID-6327760_T19",
"type": "Tissue",
"text": [
"eye muscle"
],
"offsets": [
[
1852,
1862
]
],
"normalized": []
},
{
"id": "PMID-6327760_T20",
"type": "Tissue",
"text": [
"thyroid membrane fractions"
],
"offsets": [
[
959,
985
]
],
"normalized": []
},
{
"id": "PMID-6327760_T21",
"type": "Tissue",
"text": [
"thyroid"
],
"offsets": [
[
633,
640
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-6327760_R1",
"type": "frag",
"arg1_id": "PMID-6327760_T10",
"arg2_id": "PMID-6327760_T11",
"normalized": []
},
{
"id": "PMID-6327760_R2",
"type": "frag",
"arg1_id": "PMID-6327760_T17",
"arg2_id": "PMID-6327760_T16",
"normalized": []
},
{
"id": "PMID-6327760_R3",
"type": "frag",
"arg1_id": "PMID-6327760_T21",
"arg2_id": "PMID-6327760_T5",
"normalized": []
}
] |
PMID-2777242 | PMID-2777242 | [
{
"id": "PMID-2777242__text",
"type": "abstract",
"text": [
"Anaplastic and sarcomatoid carcinoma of the small intestine: a clinicopathologic study.\nCarcinomas involving the jejunum and ileum are rare tumors. During a review of small intestinal neoplasms, six primary carcinomas of jejunum or ileum with an anaplastic and sarcomatoid histology were identified. At presentation, three of the patients had symptoms related to metastatic disease and three had symptoms referable to the local tumor. The tumors were large (greater than 4.5 cm in diameter), usually endophytic masses composed of large cells with eosinophilic cytoplasm, anaplastic nuclei, and prominent nucleoli. In many areas, the cells had a spindled configuration. Mucin positivity was identified in all six cases. Electron microscopic findings in two cases were indicative of epithelial differentiation. The tumors behaved aggressively; all five patients for whom there was clinical follow-up died of metastases within 40 months. The six anaplastic and sarcomatoid carcinomas were compared with 29 typical adenocarcinomas arising in the jejunum or ileum. Only two of the latter group had symptoms referable to distant metastases at presentation. These tumors also tended to be smaller at presentation (11 tumors were less than 4 cm in greatest dimension). Of 25 patients with typical adenocarcinomas who had acceptable follow-up, 18 (72%) died of disease and five (20%) were alive with no evidence of disease after 5 years. We conclude that anaplastic and sarcomatoid carcinoma is a rare variant of small intestinal carcinoma with an aggressive clinical course.\n"
],
"offsets": [
[
0,
1567
]
]
}
] | [
{
"id": "PMID-2777242_T1",
"type": "Pathological_formation",
"text": [
"Anaplastic and sarcomatoid carcinoma"
],
"offsets": [
[
0,
36
]
],
"normalized": []
},
{
"id": "PMID-2777242_T2",
"type": "Organ",
"text": [
"small intestine"
],
"offsets": [
[
44,
59
]
],
"normalized": []
},
{
"id": "PMID-2777242_T3",
"type": "Pathological_formation",
"text": [
"Carcinomas"
],
"offsets": [
[
88,
98
]
],
"normalized": []
},
{
"id": "PMID-2777242_T4",
"type": "Multi-tissue_structure",
"text": [
"jejunum"
],
"offsets": [
[
113,
120
]
],
"normalized": []
},
{
"id": "PMID-2777242_T5",
"type": "Multi-tissue_structure",
"text": [
"ileum"
],
"offsets": [
[
125,
130
]
],
"normalized": []
},
{
"id": "PMID-2777242_T6",
"type": "Pathological_formation",
"text": [
"tumors"
],
"offsets": [
[
140,
146
]
],
"normalized": []
},
{
"id": "PMID-2777242_T7",
"type": "Pathological_formation",
"text": [
"small intestinal neoplasms"
],
"offsets": [
[
167,
193
]
],
"normalized": []
},
{
"id": "PMID-2777242_T8",
"type": "Pathological_formation",
"text": [
"carcinomas"
],
"offsets": [
[
207,
217
]
],
"normalized": []
},
{
"id": "PMID-2777242_T9",
"type": "Multi-tissue_structure",
"text": [
"jejunum"
],
"offsets": [
[
221,
228
]
],
"normalized": []
},
{
"id": "PMID-2777242_T10",
"type": "Multi-tissue_structure",
"text": [
"ileum"
],
"offsets": [
[
232,
237
]
],
"normalized": []
},
{
"id": "PMID-2777242_T11",
"type": "Pathological_formation",
"text": [
"sarcomatoid"
],
"offsets": [
[
261,
272
]
],
"normalized": []
},
{
"id": "PMID-2777242_T12",
"type": "Pathological_formation",
"text": [
"tumor"
],
"offsets": [
[
428,
433
]
],
"normalized": []
},
{
"id": "PMID-2777242_T13",
"type": "Pathological_formation",
"text": [
"tumors"
],
"offsets": [
[
439,
445
]
],
"normalized": []
},
{
"id": "PMID-2777242_T14",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
536,
541
]
],
"normalized": []
},
{
"id": "PMID-2777242_T15",
"type": "Organism_substance",
"text": [
"eosinophilic cytoplasm"
],
"offsets": [
[
547,
569
]
],
"normalized": []
},
{
"id": "PMID-2777242_T16",
"type": "Cellular_component",
"text": [
"nuclei"
],
"offsets": [
[
582,
588
]
],
"normalized": []
},
{
"id": "PMID-2777242_T17",
"type": "Cellular_component",
"text": [
"nucleoli"
],
"offsets": [
[
604,
612
]
],
"normalized": []
},
{
"id": "PMID-2777242_T18",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
633,
638
]
],
"normalized": []
},
{
"id": "PMID-2777242_T19",
"type": "Tissue",
"text": [
"epithelial"
],
"offsets": [
[
781,
791
]
],
"normalized": []
},
{
"id": "PMID-2777242_T20",
"type": "Pathological_formation",
"text": [
"tumors"
],
"offsets": [
[
813,
819
]
],
"normalized": []
},
{
"id": "PMID-2777242_T21",
"type": "Pathological_formation",
"text": [
"metastases"
],
"offsets": [
[
906,
916
]
],
"normalized": []
},
{
"id": "PMID-2777242_T22",
"type": "Pathological_formation",
"text": [
"anaplastic and sarcomatoid carcinomas"
],
"offsets": [
[
943,
980
]
],
"normalized": []
},
{
"id": "PMID-2777242_T23",
"type": "Pathological_formation",
"text": [
"adenocarcinomas"
],
"offsets": [
[
1011,
1026
]
],
"normalized": []
},
{
"id": "PMID-2777242_T24",
"type": "Multi-tissue_structure",
"text": [
"jejunum"
],
"offsets": [
[
1042,
1049
]
],
"normalized": []
},
{
"id": "PMID-2777242_T25",
"type": "Multi-tissue_structure",
"text": [
"ileum"
],
"offsets": [
[
1053,
1058
]
],
"normalized": []
},
{
"id": "PMID-2777242_T26",
"type": "Pathological_formation",
"text": [
"metastases"
],
"offsets": [
[
1123,
1133
]
],
"normalized": []
},
{
"id": "PMID-2777242_T27",
"type": "Pathological_formation",
"text": [
"tumors"
],
"offsets": [
[
1157,
1163
]
],
"normalized": []
},
{
"id": "PMID-2777242_T28",
"type": "Pathological_formation",
"text": [
"tumors"
],
"offsets": [
[
1210,
1216
]
],
"normalized": []
},
{
"id": "PMID-2777242_T29",
"type": "Pathological_formation",
"text": [
"adenocarcinomas"
],
"offsets": [
[
1289,
1304
]
],
"normalized": []
},
{
"id": "PMID-2777242_T30",
"type": "Pathological_formation",
"text": [
"anaplastic and sarcomatoid carcinoma"
],
"offsets": [
[
1446,
1482
]
],
"normalized": []
},
{
"id": "PMID-2777242_T31",
"type": "Pathological_formation",
"text": [
"small intestinal carcinoma"
],
"offsets": [
[
1504,
1530
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-1852096-sec-05 | PMC-1852096-sec-05 | [
{
"id": "PMC-1852096-sec-05__text",
"type": "sec",
"text": [
"Case Presentation\nThe patient is an 80 year old male with diabetes mellitus and hypertension, who at age 74 (March 2001) had received a living non-related donor kidney transplant. At that time he was discharged with a double immunosuppressive therapy consisting of prednisone 20 mg/day and mophetil mycophenolate 1.5 gr/day. No calcineurin inhibitor was administered. His prednisone dose was further decreased to 5 mg/day and mophetil mycophenolate doses sustained. In November 2001 he developed cutaneous purple elevated lesions in his lower limbs that were diagnosed as KS by skin biopsy. He received 19 administrations of vincristine (1 mg) and bleomycin (15 mg) weekly that resulted in flattening and fading of the lesions. Treatment was discontinued for two months, and KS recurred, with pain and edema in both legs.\nOn July 2002, with an almost 100% involvement of his lower limbs skin with KS but no visceral involvement he received 50 mg of liposomal-adriamycin. In addition, he was then prescribed valganciclovir 450 mg BID (corrected for creatinine clearance) [7] and three additional administrations of liposomal-adriamycin, up to December 2002. He showed 40% response again with early relapse. On January 2003 the patient developed disseminated herpes zoster, which was treated with IV acyclovir.\nIn May 2003 KS progression was observed and received radiotherapy with no benefit Figure 1. In August 2003 he started oral etoposide at 50 mg QD for two weeks followed by two weeks off until May 2004 achieving a very slow 50% response. Tolerance was good and serum creatinine remain stable at around 1,4 mg/dl. Mophetil mycophenolate dose was reduced to 1 g/day and prednisone to 2.5 mg/day.\nFigure 1\nKaposi's sarcoma progressions after chemotherapy withdrawal, both lower limbs were completely covered with Kaposi's Sarcoma (June 2003).\nOn May 2004 the patient requested a second opinion and was prescribed Imatinib 200 mg qd for two weeks followed by 400 mg qd. After four weeks of Imatinib, his health deteriorated rapidly, he developed anasarca, worsening of KS, his serum creatinine increased from 1.4 mg/dl to 2.3 mg/dl and he developed grade 4 granulocytopenia (Figure 2). The patient was hospitalized with fever and was started on IV antibiotics and daily G-CSF for four days after which his WBC count normalized. Two weeks later the creatinine level returned to 1.5 mg/dl. On February 2005 he was started on 30 mg of paclitaxel IV every three weeks. After three courses with no clinical benefit he developed a skin rash that prompted discontinuation.\nFigure 2\nPatient developed anasarca with rapid progression of Kaposi's Sarcoma after four weeks of taking Imatinib (June 2004).\nOn April 2005, he was started on Sirolimus 2 mg a day, and after 8 weeks escalated to 4 mg a day. Three weeks later mophetil mycophenolate and prednisone were discontinued. Sustained and significant KS regression was evident after 16 weeks, but he developed a basal cell carcinoma and pneumonia that required hospital admission; Sirolimus dose was lowered to 2 mg a day. Thereafter his clinical course has been satisfactory with continuous and progressive regression of KS lesions (Figure 3). His serum creatinine has remained under 1.6 mg/dl and he has not developed new infectious episodes.\nFigure 3\nExtensive regression of Kaposi Sarcoma after immune-suppression was changed to Sirolimus, (14 months later), he only has hyperpigmented areas at knee levels, skin looks thin and delicate and easily bruised (July 2006).\n"
],
"offsets": [
[
0,
3518
]
]
}
] | [
{
"id": "PMC-1852096-sec-05_T1",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
161,
167
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T2",
"type": "Pathological_formation",
"text": [
"lesions"
],
"offsets": [
[
522,
529
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T3",
"type": "Organism_subdivision",
"text": [
"lower limbs"
],
"offsets": [
[
537,
548
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T4",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
578,
582
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T5",
"type": "Pathological_formation",
"text": [
"lesions"
],
"offsets": [
[
719,
726
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T6",
"type": "Pathological_formation",
"text": [
"edema"
],
"offsets": [
[
802,
807
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T7",
"type": "Organism_subdivision",
"text": [
"legs"
],
"offsets": [
[
816,
820
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T8",
"type": "Organ",
"text": [
"lower limbs skin"
],
"offsets": [
[
875,
891
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T9",
"type": "Pathological_formation",
"text": [
"KS"
],
"offsets": [
[
775,
777
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T10",
"type": "Pathological_formation",
"text": [
"KS"
],
"offsets": [
[
897,
899
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T13",
"type": "Pathological_formation",
"text": [
"Kaposi's sarcoma"
],
"offsets": [
[
1710,
1726
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T14",
"type": "Organism_subdivision",
"text": [
"lower limbs"
],
"offsets": [
[
1776,
1787
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T15",
"type": "Pathological_formation",
"text": [
"Kaposi's Sarcoma"
],
"offsets": [
[
1817,
1833
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T16",
"type": "Pathological_formation",
"text": [
"anasarca"
],
"offsets": [
[
2049,
2057
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T17",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
2080,
2085
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T11",
"type": "Cell",
"text": [
"WBC"
],
"offsets": [
[
2309,
2312
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T12",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
2528,
2532
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T18",
"type": "Pathological_formation",
"text": [
"Kaposi's Sarcoma"
],
"offsets": [
[
2631,
2647
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T19",
"type": "Pathological_formation",
"text": [
"KS"
],
"offsets": [
[
2896,
2898
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T20",
"type": "Pathological_formation",
"text": [
"basal cell carcinoma"
],
"offsets": [
[
2957,
2977
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T21",
"type": "Pathological_formation",
"text": [
"KS lesions"
],
"offsets": [
[
3167,
3177
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T22",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
3194,
3199
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T23",
"type": "Pathological_formation",
"text": [
"Kaposi Sarcoma"
],
"offsets": [
[
3323,
3337
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T24",
"type": "Organism_subdivision",
"text": [
"knee"
],
"offsets": [
[
3444,
3448
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T25",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
3457,
3461
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T26",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
1568,
1573
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T27",
"type": "Pathological_formation",
"text": [
"anasarca"
],
"offsets": [
[
2596,
2604
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T29",
"type": "Pathological_formation",
"text": [
"KS"
],
"offsets": [
[
572,
574
]
],
"normalized": []
},
{
"id": "PMC-1852096-sec-05_T30",
"type": "Pathological_formation",
"text": [
"KS"
],
"offsets": [
[
1321,
1323
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-137449-sec-08 | PMC-137449-sec-08 | [
{
"id": "PMC-137449-sec-08__text",
"type": "sec",
"text": [
"Competing interests\nNone declared.\nThis article is the third in an ongoing, educational review series on medical statistics in critical care. Previous articles have covered 'presenting and summarising data' [3] and 'samples and populations' [4]. Future topics to be covered include power calculations, comparison of means, comparison of proportions, and analysis of survival data to name but a few. If there is a medical statistics topic you would like explained contact us on editorial@ccforum.com .\n"
],
"offsets": [
[
0,
501
]
]
}
] | [] | [] | [] | [] |
PMID-8640445 | PMID-8640445 | [
{
"id": "PMID-8640445__text",
"type": "abstract",
"text": [
"Cell surface binding characteristics correlate with consensus type I interferon enhanced activity.\nThe binding characteristics of a genetically engineered consensus interferon with unusually high biologic activity were compared to the characteristics of recombinant interferon-alpha 2. Both interferon-alpha 2 and the consensus interferon produced typical biphasic Scatchard plots, indicating multiple independent binding sites. The consensus interferon, which exhibited a biologic potency more than 10-fold greater than all other type I interferons, also exhibited binding site affinities greater than those for IFN-alpha 2b. In addition, a larger number of high, and low-affinity cell surface sites were recognized by the consensus interferon, resulting in equivalent numbers of sites at reduced molar concentrations compared to IFN-a2b. Thus, at any given biologic activity, similar numbers of sites were bound by the consensus interferon and IFN-alpha 2, despite differences in their molar concentrations. No differences in internalization kinetics were identified between the two interferons, indicating that the differences in cell surface binding may be sufficient to produce the differences in biologic activity.\n"
],
"offsets": [
[
0,
1221
]
]
}
] | [
{
"id": "PMID-8640445_T1",
"type": "Cellular_component",
"text": [
"Cell surface"
],
"offsets": [
[
0,
12
]
],
"normalized": []
},
{
"id": "PMID-8640445_T2",
"type": "Cellular_component",
"text": [
"cell surface"
],
"offsets": [
[
682,
694
]
],
"normalized": []
},
{
"id": "PMID-8640445_T3",
"type": "Cellular_component",
"text": [
"cell surface"
],
"offsets": [
[
1133,
1145
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2988921-caption-02 | PMC-2988921-caption-02 | [
{
"id": "PMC-2988921-caption-02__text",
"type": "caption",
"text": [
"Selective SMA angiography was performed 5 h from onset. Before therapy, the SMA was completely occluded by an embolus at the proximal portion (a), and after the bolus infusion of urokinase (600,000 IU) into the SMA, peripheral blood flow was improved. However, the thrombus decreased in size, but remained (b). Asterisks indicate thrombus.\n"
],
"offsets": [
[
0,
340
]
]
}
] | [
{
"id": "PMC-2988921-caption-02_T1",
"type": "Organism_substance",
"text": [
"embolus"
],
"offsets": [
[
110,
117
]
],
"normalized": []
},
{
"id": "PMC-2988921-caption-02_T2",
"type": "Organism_substance",
"text": [
"bolus"
],
"offsets": [
[
161,
166
]
],
"normalized": []
},
{
"id": "PMC-2988921-caption-02_T3",
"type": "Organism_substance",
"text": [
"peripheral blood"
],
"offsets": [
[
216,
232
]
],
"normalized": []
},
{
"id": "PMC-2988921-caption-02_T4",
"type": "Organism_substance",
"text": [
"thrombus"
],
"offsets": [
[
265,
273
]
],
"normalized": []
},
{
"id": "PMC-2988921-caption-02_T5",
"type": "Organism_substance",
"text": [
"thrombus"
],
"offsets": [
[
330,
338
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2211454-sec-18 | PMC-2211454-sec-18 | [
{
"id": "PMC-2211454-sec-18__text",
"type": "sec",
"text": [
"Acknowledgements\nWe would like to thank our colleague Dr. Nikolaos Papathanasiou for his assistance in performing the statistical analysis.\n"
],
"offsets": [
[
0,
140
]
]
}
] | [] | [] | [] | [] |
PMID-15464487 | PMID-15464487 | [
{
"id": "PMID-15464487__text",
"type": "abstract",
"text": [
"Flow dynamics of the internal thoracic and radial artery T-graft.\nBACKGROUND:\nComplex use of arterial conduits has resurrected concerns about the adequacy of conduit flow. The T-graft is the extreme example of this trend. Our purpose was to identify the limitation of single source inflow and to compare flow capacity with completion coronary flow.\nMETHODS:\nBetween February 1999 and November 2001, 372 patients underwent total arterial revascularization with the T-graft alone. Intraoperative flows were recorded for each limb of the T-graft before and after distal anastomoses in 204 patients. Independent predictors of T-graft flow were identified by multivariate analysis.\nRESULTS:\nFree flow for the radial arterial (RA) limb was 161 +/- 81 mL/min, the internal thoracic artery (ITA) limb 137 +/- 57 mL/min (combined 298 +/- 101 mL/min) versus simultaneous limb flow of 226 +/- 84 mL/min giving a flow restriction of 24% +/- 14%. Completion coronary flow was 88 +/- 49 mL/min for the RA, 60 +/- 45 mL/min for the ITA, and 140 +/- 70 mL/min for both limbs simultaneously to give a flow reserve (vs simultaneous free flow) of 160% or 1.6. Independent predictors of completion RA limb flow are RA proximal diameter (p = 0.005), number of anastomoses (p = 0.018), and target stenosis (p = 0.005).\nCONCLUSIONS:\nA flow reserve of 1.6 compares favorably with an ITA flow reserve of 1.8 at 1-month postoperatively and 1.8 for both the ITA T-graft and the ITA/RA T-graft at 1-week postoperatively as reported by others. Proximal RA diameter and competitive coronary flow influence completion T-graft flow. These data quantitate the limitation of single source inflow of the T-graft configuration and support its continued use.\n"
],
"offsets": [
[
0,
1722
]
]
}
] | [
{
"id": "PMID-15464487_T2",
"type": "Multi-tissue_structure",
"text": [
"arterial conduits"
],
"offsets": [
[
93,
110
]
],
"normalized": []
},
{
"id": "PMID-15464487_T3",
"type": "Multi-tissue_structure",
"text": [
"conduit"
],
"offsets": [
[
158,
165
]
],
"normalized": []
},
{
"id": "PMID-15464487_T4",
"type": "Multi-tissue_structure",
"text": [
"coronary"
],
"offsets": [
[
334,
342
]
],
"normalized": []
},
{
"id": "PMID-15464487_T5",
"type": "Multi-tissue_structure",
"text": [
"arterial"
],
"offsets": [
[
428,
436
]
],
"normalized": []
},
{
"id": "PMID-15464487_T6",
"type": "Multi-tissue_structure",
"text": [
"radial arterial (RA) limb"
],
"offsets": [
[
704,
729
]
],
"normalized": []
},
{
"id": "PMID-15464487_T7",
"type": "Multi-tissue_structure",
"text": [
"internal thoracic artery (ITA) limb"
],
"offsets": [
[
757,
792
]
],
"normalized": []
},
{
"id": "PMID-15464487_T9",
"type": "Multi-tissue_structure",
"text": [
"coronary"
],
"offsets": [
[
945,
953
]
],
"normalized": []
},
{
"id": "PMID-15464487_T10",
"type": "Multi-tissue_structure",
"text": [
"limbs"
],
"offsets": [
[
1053,
1058
]
],
"normalized": []
},
{
"id": "PMID-15464487_T11",
"type": "Multi-tissue_structure",
"text": [
"RA limb"
],
"offsets": [
[
1178,
1185
]
],
"normalized": []
},
{
"id": "PMID-15464487_T12",
"type": "Multi-tissue_structure",
"text": [
"RA"
],
"offsets": [
[
1195,
1197
]
],
"normalized": []
},
{
"id": "PMID-15464487_T13",
"type": "Multi-tissue_structure",
"text": [
"ITA"
],
"offsets": [
[
1359,
1362
]
],
"normalized": []
},
{
"id": "PMID-15464487_T14",
"type": "Multi-tissue_structure",
"text": [
"ITA"
],
"offsets": [
[
1017,
1020
]
],
"normalized": []
},
{
"id": "PMID-15464487_T15",
"type": "Multi-tissue_structure",
"text": [
"RA"
],
"offsets": [
[
988,
990
]
],
"normalized": []
},
{
"id": "PMID-15464487_T16",
"type": "Multi-tissue_structure",
"text": [
"ITA"
],
"offsets": [
[
1431,
1434
]
],
"normalized": []
},
{
"id": "PMID-15464487_T17",
"type": "Multi-tissue_structure",
"text": [
"ITA/RA"
],
"offsets": [
[
1451,
1457
]
],
"normalized": []
},
{
"id": "PMID-15464487_T18",
"type": "Multi-tissue_structure",
"text": [
"RA"
],
"offsets": [
[
1524,
1526
]
],
"normalized": []
},
{
"id": "PMID-15464487_T19",
"type": "Multi-tissue_structure",
"text": [
"coronary"
],
"offsets": [
[
1552,
1560
]
],
"normalized": []
},
{
"id": "PMID-15464487_T8",
"type": "Multi-tissue_structure",
"text": [
"limb"
],
"offsets": [
[
861,
865
]
],
"normalized": []
},
{
"id": "PMID-15464487_T1",
"type": "Multi-tissue_structure",
"text": [
"radial artery"
],
"offsets": [
[
43,
56
]
],
"normalized": []
},
{
"id": "PMID-15464487_T22",
"type": "Multi-tissue_structure",
"text": [
"limb"
],
"offsets": [
[
523,
527
]
],
"normalized": []
},
{
"id": "PMID-15464487_T25",
"type": "Multi-tissue_structure",
"text": [
"internal thoracic"
],
"offsets": [
[
21,
38
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-15464487_R1",
"type": "frag",
"arg1_id": "PMID-15464487_T25",
"arg2_id": "PMID-15464487_T1",
"normalized": []
}
] |
PMID-899346 | PMID-899346 | [
{
"id": "PMID-899346__text",
"type": "abstract",
"text": [
"[Considerations regarding two cases of macromastia (author's transl)].\nTwo cases of macromastia have been shown; one which appeared during puberty, the other during menopause. Histopathological examination has demonstrated for the both cases a cystic degeneracy of the glandular tissue with a hyperplazia and hypertrophy of the conjunctive tissue. The pathogeny of macromastia is being discussed and it is demonstrated both the role of hypophysis hormones (prolactine and growth hormone) and of ovarian hormones (estrogens). The treatment was surgical for the both cases.\n"
],
"offsets": [
[
0,
572
]
]
}
] | [
{
"id": "PMID-899346_T1",
"type": "Tissue",
"text": [
"glandular tissue"
],
"offsets": [
[
269,
285
]
],
"normalized": []
},
{
"id": "PMID-899346_T2",
"type": "Tissue",
"text": [
"conjunctive tissue"
],
"offsets": [
[
328,
346
]
],
"normalized": []
},
{
"id": "PMID-899346_T3",
"type": "Organ",
"text": [
"ovarian"
],
"offsets": [
[
495,
502
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2889408-caption-02 | PMC-2889408-caption-02 | [
{
"id": "PMC-2889408-caption-02__text",
"type": "caption",
"text": [
"The eukaryotic parasite Trypanosoma brucei is able to import inositol from the environment or synthesize it de novo. However, according to the current model, inositol imported from the environment is utilized primarily in bulk phosphatidylinositol (red and yellow phospholipid) production via a phosphatidylinositol synthase (PIS) localized to the Golgi complex. Inositol synthesized de novo is primarily used to generate phosphatidylinositol that is used for production of glycosylphosphatidylinositols (GPIs). The de novo-synthesized inositol is believed to be utilized mostly for GPI production because the IMPase that dephosphorylates inositol 3-phosphate to inositol is localized to the ER, where GPI synthesis occurs. Mutants lacking TbINO1 are inviable because of diminished GPI production.\n"
],
"offsets": [
[
0,
798
]
]
}
] | [
{
"id": "PMC-2889408-caption-02_T1",
"type": "Cellular_component",
"text": [
"Golgi complex"
],
"offsets": [
[
348,
361
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2024775-sec-01 | PMC-2024775-sec-01 | [
{
"id": "PMC-2024775-sec-01__text",
"type": "sec",
"text": [
"Images\nFig. 1\nFig. 2\nFig. 3\n"
],
"offsets": [
[
0,
28
]
]
}
] | [] | [] | [] | [] |
PMC-2739198-caption-20 | PMC-2739198-caption-20 | [
{
"id": "PMC-2739198-caption-20__text",
"type": "caption",
"text": [
"Click here for file\n"
],
"offsets": [
[
0,
20
]
]
}
] | [] | [] | [] | [] |
PMC-2782986-sec-02 | PMC-2782986-sec-02 | [
{
"id": "PMC-2782986-sec-02__text",
"type": "sec",
"text": [
"RESEARCH DESIGN AND METHODS\nFor this study, 20 individuals (mean age 39.5 +/- 11.1 years) with long-standing type 1 diabetes (21.3 +/- 10.7 years) were enrolled in this prospective open-label crossover trial. After achieving optimal blood glucose control, 16 subjects were randomized to exenatide with or without daclizumab. Endogenous insulin production was determined by repeatedly measuring serum C-peptide.\n"
],
"offsets": [
[
0,
411
]
]
}
] | [
{
"id": "PMC-2782986-sec-02_T1",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
233,
238
]
],
"normalized": []
},
{
"id": "PMC-2782986-sec-02_T2",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
394,
399
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16650140 | PMID-16650140 | [
{
"id": "PMID-16650140__text",
"type": "abstract",
"text": [
"The ictal bradycardia syndrome: localization and lateralization.\nPURPOSE:\nPrevious studies have established the importance of the insular cortex and temporal lobe in cardiovascular autonomic modulation. Some investigators, based on the results of cortical stimulation response, functional imaging, EEG recordings of seizures, and lesional studies, have suggested that cardiac sympathetic and parasympathetic function may be lateralized, with sympathetic representation lateralized to the right insula, and parasympathetic, to the left. These studies have suggested that ictal bradycardia is most commonly a manifestation of activation of the left temporal and insular cortex. However, the evidence for this is inconsistent. We sought to assess critically the predictable value of ictal bradycardia for seizure localization and lateralization.\nMETHODS:\nIn this study, we reviewed the localization of seizure activity in 13 consecutive patients with ictal bradycardia diagnosed during prolonged video-EEG monitoring at Mayo Clinic Rochester. The localization of electrographic seizure activity at seizure onset and bradycardia onset was identified in all patients. In addition, we performed a comprehensive review of the ictal bradycardia literature focusing on localization of seizure activity in ictal bradycardia cases.\nRESULTS:\nAll occurrences of ictal bradycardia in the 13 identified patients were associated with temporal lobe-onset seizures. However, no consistent lateralization of seizure activity was found at onset of seizure activity or at onset of bradycardia in this population. Seizure activity was bilateral at bradycardia onset in nine of 13 patients. The results from the literature review also showed that a predominance of patients had bilateral activity at bradycardia onset; however, more of the ictal bradycardia cases from the literature had left hemispheric localization of seizure onset.\nCONCLUSIONS:\nIctal bradycardia most often occurs in association with bilateral hemispheric seizure activity and is not a consistent lateralizing sign in localizing seizure onset. Our data do not support the existence of a strictly unilateral parasympathetic cardiomotor representation in the left hemisphere, as has been suggested.\n"
],
"offsets": [
[
0,
2245
]
]
}
] | [
{
"id": "PMID-16650140_T1",
"type": "Multi-tissue_structure",
"text": [
"insular cortex"
],
"offsets": [
[
130,
144
]
],
"normalized": []
},
{
"id": "PMID-16650140_T2",
"type": "Multi-tissue_structure",
"text": [
"temporal lobe"
],
"offsets": [
[
149,
162
]
],
"normalized": []
},
{
"id": "PMID-16650140_T3",
"type": "Multi-tissue_structure",
"text": [
"cortical"
],
"offsets": [
[
247,
255
]
],
"normalized": []
},
{
"id": "PMID-16650140_T4",
"type": "Multi-tissue_structure",
"text": [
"right insula"
],
"offsets": [
[
488,
500
]
],
"normalized": []
},
{
"id": "PMID-16650140_T5",
"type": "Multi-tissue_structure",
"text": [
"left"
],
"offsets": [
[
530,
534
]
],
"normalized": []
},
{
"id": "PMID-16650140_T6",
"type": "Multi-tissue_structure",
"text": [
"left temporal"
],
"offsets": [
[
642,
655
]
],
"normalized": []
},
{
"id": "PMID-16650140_T7",
"type": "Multi-tissue_structure",
"text": [
"insular cortex"
],
"offsets": [
[
660,
674
]
],
"normalized": []
},
{
"id": "PMID-16650140_T8",
"type": "Anatomical_system",
"text": [
"cardiovascular"
],
"offsets": [
[
166,
180
]
],
"normalized": []
},
{
"id": "PMID-16650140_T9",
"type": "Multi-tissue_structure",
"text": [
"left hemispheric"
],
"offsets": [
[
1865,
1881
]
],
"normalized": []
},
{
"id": "PMID-16650140_T10",
"type": "Organ",
"text": [
"cardiac"
],
"offsets": [
[
368,
375
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-16650140_R1",
"type": "frag",
"arg1_id": "PMID-16650140_T5",
"arg2_id": "PMID-16650140_T4",
"normalized": []
},
{
"id": "PMID-16650140_R2",
"type": "frag",
"arg1_id": "PMID-16650140_T6",
"arg2_id": "PMID-16650140_T7",
"normalized": []
}
] |
PMC-2690976-sec-05 | PMC-2690976-sec-05 | [
{
"id": "PMC-2690976-sec-05__text",
"type": "sec",
"text": [
"Efficacy of MMF in current immunosuppressive regimens after kidney transplantation\nCurrent established immunosuppressive strategies in kidney transplantation often include an induction agent (monoclonal or polyclonal anti-T-cell antibodies) based on the immunologic risk of the recipient, followed by a maintenance regimen combining a CNI and an anti-proliferative agent, with or without corticosteroids.2-4 As MMF was the first MPA formulation approved in clinical kidney transplantation, more extensive clinical data are available with this drug in comparison to EC-MPS.\n\n"
],
"offsets": [
[
0,
574
]
]
}
] | [
{
"id": "PMC-2690976-sec-05_T1",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
60,
66
]
],
"normalized": []
},
{
"id": "PMC-2690976-sec-05_T2",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
135,
141
]
],
"normalized": []
},
{
"id": "PMC-2690976-sec-05_T3",
"type": "Cell",
"text": [
"T-cell"
],
"offsets": [
[
222,
228
]
],
"normalized": []
},
{
"id": "PMC-2690976-sec-05_T4",
"type": "Organ",
"text": [
"kidney"
],
"offsets": [
[
466,
472
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-9088383 | PMID-9088383 | [
{
"id": "PMID-9088383__text",
"type": "abstract",
"text": [
"Procedural memory stimulation in Alzheimer's disease: impact of a training programme.\nThe study evaluates the efficacy of a procedural memory stimulation programme in mild and mild-moderate Alzheimer's disease (AD). Twenty basic and instrumental activities of daily living have been selected, and divided into two groups, comparable for difficulty. Ten normal elderly subjects (age 68.0 +/- 4.8 years; MMSE score: 28.7 +/- 0.9; education: 7.6 +/- 3.5 years) were asked to perform the two groups of daily activities and the time required to perform the tasks of each group was recorded and used as a reference. Ten mild and mild-moderate AD patients (age 77.2 +/- 5.3 years; MMSE score: 19.8 +/- 3.5; education: 7.3 +/- 4.7 years) without major behavioural disturbances constituted the experimental group. Patients were evaluated in all 20 daily activities and the time employed was recorded at baseline and after a 3-week training (1 h/d, 5 d/week) period. Five patients were trained during the 3 weeks on half of the 20 daily activities and the other five patients were trained on the remainder. This procedure was adopted in order to detect separately the improvement in \"trained\" and \"not trained\" activities, allowing to control better the effects of the intervention. The assessment of the functional impact of the training was directly measured, through the variation of time employed to perform tasks before and after training. After 3 weeks of training a significant improvement was observed for the trained activities, from 3.6 to 1.9 standard deviations below the performance of the normal elderly controls (P < 0.05). AD patients improved also in not-trained activities from 3.5 to 2.7 standard deviations below the controls' performance (P < 0.05). The rehabilitation of activities of daily living through developing procedural memory strategies may be effective in mild and mild-moderate AD patients.\n"
],
"offsets": [
[
0,
1914
]
]
}
] | [] | [] | [] | [] |
PMC-2713402-sec-09 | PMC-2713402-sec-09 | [
{
"id": "PMC-2713402-sec-09__text",
"type": "sec",
"text": [
"Statistical Analysis\nMitochondrial DNA haplogroup frequencies were calculated by counting from the observed genotypes. The Pearson chi-square test and the chi-square test for linear-by-linear association were used to analyze the significances between the prevalence of haplogroups and different age groups. SPSS software (version 10.0) was used.\n"
],
"offsets": [
[
0,
346
]
]
}
] | [
{
"id": "PMC-2713402-sec-09_T1",
"type": "Cellular_component",
"text": [
"Mitochondrial"
],
"offsets": [
[
21,
34
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-14981916 | PMID-14981916 | [
{
"id": "PMID-14981916__text",
"type": "abstract",
"text": [
"Full sequencing analysis of estrogen receptor-alpha gene polymorphism and its association with breast cancer risk.\nBACKGROUND:\nThe estrogen receptor plays a critical role in breast cancer development and progression. So the genetic polymorphism of ER-alpha gene could affect cancer risk and phenotype.\nMATERIALS AND METHODS:\nWe fully sequenced the ER-alpha gene to investigate its single nucleotide polymorphisms (SNPs) in 100 breast cancer patients and 100 controls.\nRESULTS:\nSix novel polymorphism in the control and 11 in cancer patients were found. The G/G genotype at C975 G and A/A genotype at G1782 A had a protective effect against breast cancer when compared to other genotypes (OR = 0.3 and 0.3, respectively). 975G allele was associated inversely with the p53 expression and positively with the bcl-2 expression in cancer with borderline significance. Combining this result with our previous study, these associations became more significant (p = 0.005 and 0.019, respectively).\nCONCLUSION:\nPolymorphisms in ER-alpha gene can affect the breast cancer susceptibility and may be related to other protein expression, such as p53 and bcl-2.\n"
],
"offsets": [
[
0,
1148
]
]
}
] | [
{
"id": "PMID-14981916_T1",
"type": "Pathological_formation",
"text": [
"breast cancer"
],
"offsets": [
[
95,
108
]
],
"normalized": []
},
{
"id": "PMID-14981916_T2",
"type": "Pathological_formation",
"text": [
"breast cancer"
],
"offsets": [
[
174,
187
]
],
"normalized": []
},
{
"id": "PMID-14981916_T3",
"type": "Pathological_formation",
"text": [
"cancer"
],
"offsets": [
[
275,
281
]
],
"normalized": []
},
{
"id": "PMID-14981916_T4",
"type": "Pathological_formation",
"text": [
"breast cancer"
],
"offsets": [
[
427,
440
]
],
"normalized": []
},
{
"id": "PMID-14981916_T5",
"type": "Pathological_formation",
"text": [
"cancer"
],
"offsets": [
[
525,
531
]
],
"normalized": []
},
{
"id": "PMID-14981916_T6",
"type": "Pathological_formation",
"text": [
"breast cancer"
],
"offsets": [
[
640,
653
]
],
"normalized": []
},
{
"id": "PMID-14981916_T7",
"type": "Pathological_formation",
"text": [
"cancer"
],
"offsets": [
[
826,
832
]
],
"normalized": []
},
{
"id": "PMID-14981916_T8",
"type": "Pathological_formation",
"text": [
"breast cancer"
],
"offsets": [
[
1048,
1061
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2646243-sec-01 | PMC-2646243-sec-01 | [
{
"id": "PMC-2646243-sec-01__text",
"type": "sec",
"text": [
"Background\n\n"
],
"offsets": [
[
0,
12
]
]
}
] | [] | [] | [] | [] |
PMID-14729736 | PMID-14729736 | [
{
"id": "PMID-14729736__text",
"type": "abstract",
"text": [
"Antibiotic-induced persistence of cytotoxic Staphylococcus aureus in non-phagocytic cells.\nOBJECTIVES:\nAfter infection of non-phagocytic cells, some Staphylococcus aureus strains are able to survive and kill their host cells. The purpose of this study was to determine the action of various antibiotics on the survival of host cells and/or intracellular S. aureus.\nMETHODS:\nMurine keratinocyte (PAM212) and fibroblast (mKSA) cell lines were infected with cytotoxic S. aureus and cultured in the presence of various antibiotics at graded concentrations. The viability of host cells was measured 24 h after infection. To determine the bacterial viability within host cells, cellular lysates were prepared and colony forming units were quantified using a spiral plater. Host cells infected with fluorescein isothiocyanate (FITC)-labelled S. aureus were analysed by flow cytometry and microscopy to determine the subcellular localization S. aureus.\nRESULTS:\nOxacillin, vancomycin, gentamicin, ciprofloxacin and trimethoprim/sulfamethoxazole did not rescue host cells from cell death induced by intracellular S. aureus. In contrast, linezolid, rifampicin, azithromycin, clindamycin, erythromycin and quinupristin/dalfopristin suppressed the cytotoxic action of S. aureus. After withdrawal of antibiotics, intracellular S. aureus regained cytotoxic activity and killed their host cells. Only rifampicin was able to eliminate intracellular S. aureus completely within 72 h. In contrast, clindamycin, azithromycin and linezolid induced a state of intracellular persistence of viable S. aureus.\nCONCLUSIONS:\nAntibiotics commonly used for the management of S. aureus infections appear to create a niche for invasive intracellular S. aureus, which may play an important role for persistence and recurrence of infection. Because of its unique ability to eliminate intracellular S. aureus, rifampicin appears to be valuable for the treatment of invasive S. aureus infections.\n"
],
"offsets": [
[
0,
1963
]
]
}
] | [
{
"id": "PMID-14729736_T1",
"type": "Cell",
"text": [
"non-phagocytic cells"
],
"offsets": [
[
69,
89
]
],
"normalized": []
},
{
"id": "PMID-14729736_T2",
"type": "Cell",
"text": [
"non-phagocytic cells"
],
"offsets": [
[
122,
142
]
],
"normalized": []
},
{
"id": "PMID-14729736_T3",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
219,
224
]
],
"normalized": []
},
{
"id": "PMID-14729736_T4",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
327,
332
]
],
"normalized": []
},
{
"id": "PMID-14729736_T5",
"type": "Cell",
"text": [
"keratinocyte"
],
"offsets": [
[
381,
393
]
],
"normalized": []
},
{
"id": "PMID-14729736_T6",
"type": "Cell",
"text": [
"PAM212"
],
"offsets": [
[
395,
401
]
],
"normalized": []
},
{
"id": "PMID-14729736_T7",
"type": "Cell",
"text": [
"fibroblast"
],
"offsets": [
[
407,
417
]
],
"normalized": []
},
{
"id": "PMID-14729736_T8",
"type": "Cell",
"text": [
"mKSA) cell lines"
],
"offsets": [
[
419,
435
]
],
"normalized": []
},
{
"id": "PMID-14729736_T9",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
575,
580
]
],
"normalized": []
},
{
"id": "PMID-14729736_T10",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
665,
670
]
],
"normalized": []
},
{
"id": "PMID-14729736_T11",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
772,
777
]
],
"normalized": []
},
{
"id": "PMID-14729736_T12",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
1057,
1062
]
],
"normalized": []
},
{
"id": "PMID-14729736_T13",
"type": "Cell",
"text": [
"cell"
],
"offsets": [
[
1068,
1072
]
],
"normalized": []
},
{
"id": "PMID-14729736_T14",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
1374,
1379
]
],
"normalized": []
},
{
"id": "PMID-14729736_T16",
"type": "Organism_substance",
"text": [
"cellular lysates"
],
"offsets": [
[
672,
688
]
],
"normalized": []
},
{
"id": "PMID-14729736_T17",
"type": "Cellular_component",
"text": [
"subcellular"
],
"offsets": [
[
909,
920
]
],
"normalized": []
},
{
"id": "PMID-14729736_T15",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
340,
353
]
],
"normalized": []
},
{
"id": "PMID-14729736_T18",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1090,
1103
]
],
"normalized": []
},
{
"id": "PMID-14729736_T19",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1300,
1313
]
],
"normalized": []
},
{
"id": "PMID-14729736_T20",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1419,
1432
]
],
"normalized": []
},
{
"id": "PMID-14729736_T21",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1539,
1552
]
],
"normalized": []
},
{
"id": "PMID-14729736_T22",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1706,
1719
]
],
"normalized": []
},
{
"id": "PMID-14729736_T23",
"type": "Immaterial_anatomical_entity",
"text": [
"intracellular"
],
"offsets": [
[
1852,
1865
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-14729736_R1",
"type": "frag",
"arg1_id": "PMID-14729736_T6",
"arg2_id": "PMID-14729736_T8",
"normalized": []
}
] |
PMID-12344153 | PMID-12344153 | [
{
"id": "PMID-12344153__text",
"type": "abstract",
"text": [
"Act No. 16.045 of 2 June 1989 prohibiting all discrimination that violates the principle of equality of treatment and opportunities for both sexes in all sectors of labor activity.\nThis Uruguayan Act prohibits discrimination in employment with respect to the following areas, among others: 1) advertising for the provision of positions; 2) selection criteria; 3) recruitment and hiring; 4) evaluation of performance criteria; 5) the right to advancement and promotion; 6) labour stability; 7) social benefits; 8) suspension and dismissal, particularly in cases involving a change of civil status, pregnancy, or nursing; 9) possibilities for professional and technical education or retraining; and 10) remuneration criteria. Reserving places for one sex because of the presence of activities in which the sex of the employee is essential for performance or to comply with international labor treaties does not constitute discrimination. Nor do compensatory acts designed to promote equality of opportunities and treatment of both sexes in concrete situations. In cases where the provisions of this Act have been violated, specially designated judges will call the parties together and may adopt measures designed to end the situation complained of. If they deem it necessary, the judges may institute more formal proceedings. If the measures adopted are not carried out, the person violating the law is subject to a daily fine, as well as administrative penalties set out in Act 15.903 of 10 November 1987. Adverse decisions may be appealed. The state is also to undertake educative campaigns to create interest in and understanding of the problems affecting women workers, thus promoting awareness in such workers and their employers of their situation.\n"
],
"offsets": [
[
0,
1760
]
]
}
] | [] | [] | [] | [] |
PMID-7684185 | PMID-7684185 | [
{
"id": "PMID-7684185__text",
"type": "abstract",
"text": [
"Comparative immunohistochemical study of primary and metastatic carcinomas of the liver.\nDistinguishing primary hepatocellular carcinoma (HCC) from metastatic carcinomas to the liver is often difficult, if not impossible, particularly in needle biopsy and fine-needle aspiration specimens. In an attempt to identify a specific immunohistochemical profile that would distinguish HCC from metastatic carcinomas, we studied 56 HCCs, 8 cholangiocarcinomas, and 24 metastatic adenocarcinomas with monoclonal antibodies to alpha-fetoprotein (AFP), keratin (AE1, AE3, and CAM5.2), Leu-M1, human milk fat globule (HMFG-2), tumor-associated glycoprotein-72(B72.3), epithelial specific membrane antigen (Ber-EP4), and BCA-225 (CU-18). Both monoclonal and polyclonal (mCEA and pCEA) antibodies to carcinoembryonic antigen also were used. Metastatic adenocarcinomas were often positive for CU-18(71%), Leu-M1 (75%), B72.3 (50%), HMFG-2 (67%), Ber-EP4(83%) and mCEA(71%). Using these antibodies, the frequency of positivity for HCC was 9%, 16%, 11%, 20%, 36%, and 11%, respectively. CU-18 was the only monoclonal antibody in which there was a significant difference in positive rates between HCC and metastatic adenocarcinomas. Most HCCs (71%) revealed a bile canalicular staining pattern with pCEA. Because this staining pattern was absent in metastatic carcinomas, pCEA appears to be useful in confirming a diagnosis of HCC. AE1, AE3 and CAM5.2 antibodies were not useful in distinguishing HCC from metastatic carcinomas. Each cholangiocarcinoma shared a staining profile similar to that of metastatic carcinomas.\n"
],
"offsets": [
[
0,
1603
]
]
}
] | [
{
"id": "PMID-7684185_T1",
"type": "Pathological_formation",
"text": [
"primary"
],
"offsets": [
[
41,
48
]
],
"normalized": []
},
{
"id": "PMID-7684185_T2",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
53,
74
]
],
"normalized": []
},
{
"id": "PMID-7684185_T3",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
82,
87
]
],
"normalized": []
},
{
"id": "PMID-7684185_T4",
"type": "Pathological_formation",
"text": [
"primary hepatocellular carcinoma"
],
"offsets": [
[
104,
136
]
],
"normalized": []
},
{
"id": "PMID-7684185_T5",
"type": "Pathological_formation",
"text": [
"HCC"
],
"offsets": [
[
138,
141
]
],
"normalized": []
},
{
"id": "PMID-7684185_T6",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
148,
169
]
],
"normalized": []
},
{
"id": "PMID-7684185_T7",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
177,
182
]
],
"normalized": []
},
{
"id": "PMID-7684185_T8",
"type": "Multi-tissue_structure",
"text": [
"needle biopsy"
],
"offsets": [
[
238,
251
]
],
"normalized": []
},
{
"id": "PMID-7684185_T9",
"type": "Multi-tissue_structure",
"text": [
"fine-needle aspiration specimens"
],
"offsets": [
[
256,
288
]
],
"normalized": []
},
{
"id": "PMID-7684185_T10",
"type": "Pathological_formation",
"text": [
"HCC"
],
"offsets": [
[
378,
381
]
],
"normalized": []
},
{
"id": "PMID-7684185_T11",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
387,
408
]
],
"normalized": []
},
{
"id": "PMID-7684185_T12",
"type": "Pathological_formation",
"text": [
"cholangiocarcinomas"
],
"offsets": [
[
432,
451
]
],
"normalized": []
},
{
"id": "PMID-7684185_T13",
"type": "Pathological_formation",
"text": [
"metastatic adenocarcinomas"
],
"offsets": [
[
460,
486
]
],
"normalized": []
},
{
"id": "PMID-7684185_T15",
"type": "Pathological_formation",
"text": [
"tumor"
],
"offsets": [
[
615,
620
]
],
"normalized": []
},
{
"id": "PMID-7684185_T16",
"type": "Tissue",
"text": [
"epithelial"
],
"offsets": [
[
656,
666
]
],
"normalized": []
},
{
"id": "PMID-7684185_T17",
"type": "Cellular_component",
"text": [
"membrane"
],
"offsets": [
[
676,
684
]
],
"normalized": []
},
{
"id": "PMID-7684185_T19",
"type": "Pathological_formation",
"text": [
"Metastatic adenocarcinomas"
],
"offsets": [
[
827,
853
]
],
"normalized": []
},
{
"id": "PMID-7684185_T20",
"type": "Pathological_formation",
"text": [
"HCC"
],
"offsets": [
[
1015,
1018
]
],
"normalized": []
},
{
"id": "PMID-7684185_T21",
"type": "Pathological_formation",
"text": [
"HCC"
],
"offsets": [
[
1179,
1182
]
],
"normalized": []
},
{
"id": "PMID-7684185_T22",
"type": "Pathological_formation",
"text": [
"metastatic adenocarcinomas"
],
"offsets": [
[
1187,
1213
]
],
"normalized": []
},
{
"id": "PMID-7684185_T23",
"type": "Pathological_formation",
"text": [
"HCCs"
],
"offsets": [
[
1220,
1224
]
],
"normalized": []
},
{
"id": "PMID-7684185_T24",
"type": "Multi-tissue_structure",
"text": [
"bile canalicular"
],
"offsets": [
[
1242,
1258
]
],
"normalized": []
},
{
"id": "PMID-7684185_T25",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
1331,
1352
]
],
"normalized": []
},
{
"id": "PMID-7684185_T26",
"type": "Pathological_formation",
"text": [
"HCC"
],
"offsets": [
[
1479,
1482
]
],
"normalized": []
},
{
"id": "PMID-7684185_T27",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
1488,
1509
]
],
"normalized": []
},
{
"id": "PMID-7684185_T28",
"type": "Pathological_formation",
"text": [
"cholangiocarcinoma"
],
"offsets": [
[
1516,
1534
]
],
"normalized": []
},
{
"id": "PMID-7684185_T29",
"type": "Pathological_formation",
"text": [
"metastatic carcinomas"
],
"offsets": [
[
1580,
1601
]
],
"normalized": []
}
] | [] | [
{
"id": "PMID-7684185_1",
"entity_ids": [
"PMID-7684185_T4",
"PMID-7684185_T5"
]
}
] | [
{
"id": "PMID-7684185_R1",
"type": "frag",
"arg1_id": "PMID-7684185_T1",
"arg2_id": "PMID-7684185_T2",
"normalized": []
},
{
"id": "PMID-7684185_R2",
"type": "Part-of",
"arg1_id": "PMID-7684185_T2",
"arg2_id": "PMID-7684185_T3",
"normalized": []
},
{
"id": "PMID-7684185_R3",
"type": "Part-of",
"arg1_id": "PMID-7684185_T6",
"arg2_id": "PMID-7684185_T7",
"normalized": []
},
{
"id": "PMID-7684185_R4",
"type": "frag",
"arg1_id": "PMID-7684185_T8",
"arg2_id": "PMID-7684185_T9",
"normalized": []
}
] |
PMC-2268729-sec-08 | PMC-2268729-sec-08 | [
{
"id": "PMC-2268729-sec-08__text",
"type": "sec",
"text": [
"Ovariectomy\nBased on the uterine weight, we determined seven unsuccessful OVXs. The rats concerned were removed from further analyses, which left nine rats in the control group, five in the OVX group, seven in the OVX and late ZOL group, and eight in the OVX and early ZOL group. For each animal, we determined the percentage change in structural parameters compared to the values at week 0. Figure 1 shows the average percentage change and upper standard deviation for all groups for BV/TV, Conn.D, SMI, Tb.N, Tb.Th, and Tb.Sp. The OVX group without treatment showed large changes in structural parameters, indicating the development of OVX-induced bone loss (Figs. 1 and 2). Paired Student's t-test indicated significant changes within 2 weeks after OVX for all structural parameters. BV/TV, Conn.D, and Tb.N decreased during the experiment and SMI and Tb.Sp increased. Both Tb.Th and Tb.N decreased within 2 weeks, indicating that both thinning and complete resorption of trabeculae started directly after OVX. The initial rapid loss of bone and connectivity was largely accompanied by trabecular thinning, while secondary, slower loss of bone was concomitant with a decrease in Tb.N. While BV/TV, Conn.D, SMI, Tb.N, and Tb.Sp showed continuous changes in the same direction throughout the experiment, Tb.Th initially decreased significantly until 4 weeks after OVX and then increased again until after 16 weeks Tb.Th was significantly higher than in the control group. \nFig. 1\nAverage percentage change in structural parameters in the metaphyseal proximal tibia and upper standard deviation for all groups at all time points. Brackets indicate P < 0.05 at week 16\nFig. 2\nSame slice of an unprocessed CT scan of the same rat in the OVX group taken at weeks 0 (a), 2 (b), 4 (c), 8 (d), 12 (e), and 16 (f). Images show typical trabecular bone loss due to OVX in the metaphysis. Green line shows the analyzed metaphyseal bone\nThe absolute average values and standard deviations for all structural parameters of all measurements are shown in Table 1. At the starting point, some differences in the values between the groups were present. This was due to the fact that some animals, which mostly had a relatively low BV/TV, were removed from the study because they did not respond to the OVX. However, since we compared the relative changes in each animal, the results were most likely not affected by the difference in absolute values. \nTable 1\nMean values and standard deviation of all structural parameters of all groups at the start of the experiment\nGroup BV/TV (1) Conn.D (1/mm) SMI (1) Tb.N (1/mm) Tb.Th (mum) Tb.Sp (mum)\nControl 0.17 (0.056) 41 (47) 1.52 (0.53) 1.89 (1.38) 105 (49) 613 (368)\nOVX 0.26 (0.055) 141 (76) 1.22 (0.39) 3.77 (1.66) 84 (10) 335 (174)\nOVX + late ZOL 0.23 (0.062) 86 (66) 1.23 (0.34) 2.77 (1.55) 89 (13) 482 (227)\nOVX + early ZOL 0.17 (0.056) 38 (21) 1.70 (0.39) 1.86 (0.80) 95 (7) 647 (207)\n"
],
"offsets": [
[
0,
2923
]
]
}
] | [
{
"id": "PMC-2268729-sec-08_T1",
"type": "Organ",
"text": [
"uterine"
],
"offsets": [
[
25,
32
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T2",
"type": "Tissue",
"text": [
"bone"
],
"offsets": [
[
1040,
1044
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T3",
"type": "Organ",
"text": [
"trabecular"
],
"offsets": [
[
1089,
1099
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T4",
"type": "Tissue",
"text": [
"bone"
],
"offsets": [
[
1142,
1146
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T5",
"type": "Organ",
"text": [
"tibia"
],
"offsets": [
[
1560,
1565
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T7",
"type": "Tissue",
"text": [
"trabecular bone"
],
"offsets": [
[
1828,
1843
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T8",
"type": "Tissue",
"text": [
"bone"
],
"offsets": [
[
1921,
1925
]
],
"normalized": []
},
{
"id": "PMC-2268729-sec-08_T6",
"type": "Tissue",
"text": [
"bone"
],
"offsets": [
[
650,
654
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2535566-caption-18 | PMC-2535566-caption-18 | [
{
"id": "PMC-2535566-caption-18__text",
"type": "caption",
"text": [
"Click here for additional data file.\n"
],
"offsets": [
[
0,
37
]
]
}
] | [] | [] | [] | [] |
PMC-1971061-sec-09 | PMC-1971061-sec-09 | [
{
"id": "PMC-1971061-sec-09__text",
"type": "sec",
"text": [
"Etiology\nAnorectal malformations (ARM) represent a spectrum of abnormalities ranging from mild anal anomalies to complex cloacal malformations. The etiology of such malformations remains unclear and is likely multifactorial. There are however reasons to believe there is a genetic componenet. As early as the 1950s, it was recognized that there was an increased risk for a sibling of a patient with ARM to be born with a malformation, as much as 1 in 100, compared with the incidence of about 1 in 5000 in the general population. Since that time there have been reports of families with 2 or more affected members and associations of ARMs with multisystem syndromes. In particular, mutations in specific genes encoding transcription factors have been described in patients having Townes-Broks syndrome, Currarino's syndrome, and Pallister-Hall syndrome, each of which have autosomal dominant modes of inheritance. In addition, it has been found that there is not only an increased incidence of ARM in patient with trisomy 21 (Down's syndrome), but that 95% of patients with trisomy 21 and ARM have imperforate anus without fistula, compared with only 5% of all patients with ARM. Based on this evidence, it is likely that the mutation of a variety of different genes can result in ARM, or that the etiology of ARM is multigenic [13].\n"
],
"offsets": [
[
0,
1334
]
]
}
] | [
{
"id": "PMC-1971061-sec-09_T1",
"type": "Organism_subdivision",
"text": [
"Anorectal"
],
"offsets": [
[
9,
18
]
],
"normalized": []
},
{
"id": "PMC-1971061-sec-09_T2",
"type": "Immaterial_anatomical_entity",
"text": [
"anal"
],
"offsets": [
[
95,
99
]
],
"normalized": []
},
{
"id": "PMC-1971061-sec-09_T3",
"type": "Immaterial_anatomical_entity",
"text": [
"anus"
],
"offsets": [
[
1110,
1114
]
],
"normalized": []
},
{
"id": "PMC-1971061-sec-09_T4",
"type": "Pathological_formation",
"text": [
"fistula"
],
"offsets": [
[
1123,
1130
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2217075-caption-07 | PMC-2217075-caption-07 | [
{
"id": "PMC-2217075-caption-07__text",
"type": "caption",
"text": [
"Anion to cation selectivity ratio determined from the relative rates of reaction of MTSES- and MTSET+ with the water exposed residues in the M6 segment. The anion selectivity ratio is calculated as described in Table II, column 5. Note the marked increase in anion selectivity at the residues T351C and Q353C. A ratio of 1 indicates no selectivity between anions and cations. The larger the ratio the greater the anion selectivity.\n"
],
"offsets": [
[
0,
432
]
]
}
] | [] | [] | [] | [] |
PMID-9394578 | PMID-9394578 | [
{
"id": "PMID-9394578__text",
"type": "abstract",
"text": [
"[Extra-anatomic bypass from the ascending aorta to the supraceliac abdominal aorta--surgical option applied to reoperation for aortic coarctation or interruption].\nThe optimal approach for reoperation following repair of aortic coarctation (CoA) or interruption (IAA) remains controversial. Four patients underwent extra-anatomic bypass for restenosis after repair of CoA or IAA. The age ranged from 4 to 12 years. The initial repairs for two CoA, one type A-IAA, and one type B-IAA consisted of two grafting, one subclavian arterial turning-down aortoplasty, and one subclavian flap aortoplasty. All of them underwent during infancy. Preoperative right arm systolic pressure ranged from 140 to 190 mmHg ar rest. Through a midline sternotomy and an upper laparotmy incision, an extra-anatomic bypass from the ascending aorta to the supraceliac abdominal aorta was employed using a 12 to 18 mm tube graft. All patients survived surgeries, and their hypertension markedly improved. Our experience confirms safety and effectiveness of this option in selected young patients with re-stenosis of following repair of CoA or IAA.\n"
],
"offsets": [
[
0,
1123
]
]
}
] | [
{
"id": "PMID-9394578_T1",
"type": "Multi-tissue_structure",
"text": [
"abdominal aorta"
],
"offsets": [
[
67,
82
]
],
"normalized": []
},
{
"id": "PMID-9394578_T2",
"type": "Multi-tissue_structure",
"text": [
"aortic"
],
"offsets": [
[
221,
227
]
],
"normalized": []
},
{
"id": "PMID-9394578_T3",
"type": "Multi-tissue_structure",
"text": [
"arterial"
],
"offsets": [
[
525,
533
]
],
"normalized": []
},
{
"id": "PMID-9394578_T4",
"type": "Organism_subdivision",
"text": [
"right arm"
],
"offsets": [
[
648,
657
]
],
"normalized": []
},
{
"id": "PMID-9394578_T5",
"type": "Multi-tissue_structure",
"text": [
"abdominal aorta"
],
"offsets": [
[
844,
859
]
],
"normalized": []
},
{
"id": "PMID-9394578_T7",
"type": "Multi-tissue_structure",
"text": [
"aortic"
],
"offsets": [
[
127,
133
]
],
"normalized": []
},
{
"id": "PMID-9394578_T8",
"type": "Multi-tissue_structure",
"text": [
"flap"
],
"offsets": [
[
579,
583
]
],
"normalized": []
},
{
"id": "PMID-9394578_T9",
"type": "Multi-tissue_structure",
"text": [
"ascending aorta"
],
"offsets": [
[
809,
824
]
],
"normalized": []
},
{
"id": "PMID-9394578_T10",
"type": "Multi-tissue_structure",
"text": [
"ascending aorta"
],
"offsets": [
[
32,
47
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-1683740 | PMID-1683740 | [
{
"id": "PMID-1683740__text",
"type": "abstract",
"text": [
"Changes of lymphocyte subsets in leukemia patients who received allogenic bone marrow transplantation.\nProportional changes of lymphocyte subsets in the peripheral blood were monitored by two-color flow-cytometry in seven leukemia patients who had received allogenic bone marrow transplantation (BMT). Lymphocyte counts, and proportions of T and B-cells returned to normal ranges between the 2nd and 12th months after BMT. Activated T-cells prominently increased after BMT, and the values gradually returned toward normal. As to lymphocyte subsets, the proportions of CD 4+ cells had remained low, while those of CD 8+ cells high for a whole observation period after BMT. The changes of CD 4+ cells were caused by the decrease of suppressor-inducer T-cells (CD 4+ Leu 8+). High proportion of CD 8+ cells was mainly associated with increased suppressor T-cells (CD 8+ CD 11+). Among natural killer (NK) cells, highly active NK cells (CD 16+ CD 57-) markedly increased shortly after BMT, and gradually returned to normal. CD 16 -CD 57+ NK cells increased beyond normal ranges after the 2nd month. The incidence or degree of acute and chronic graft-versus-host diseases (GVHD) did not correlate with the changes of any lymphocyte subsets. The present results suggest that the increase of activated T-cells shortly after BMT reflects lymphocyte reconstitution. The prolonged immune deficiency after BMT might be related to either deficient expression of homing receptor (Leu 8 antigen) on CD 4+ cells or increased suppressor T-cells (CD 8+ CD 11+). In addition, the early increase of NK cells after BMT may compensate for the immune deficiency in BMT patients.\n"
],
"offsets": [
[
0,
1657
]
]
}
] | [
{
"id": "PMID-1683740_T1",
"type": "Cell",
"text": [
"lymphocyte"
],
"offsets": [
[
11,
21
]
],
"normalized": []
},
{
"id": "PMID-1683740_T2",
"type": "Multi-tissue_structure",
"text": [
"bone marrow"
],
"offsets": [
[
74,
85
]
],
"normalized": []
},
{
"id": "PMID-1683740_T3",
"type": "Cell",
"text": [
"lymphocyte"
],
"offsets": [
[
127,
137
]
],
"normalized": []
},
{
"id": "PMID-1683740_T4",
"type": "Organism_substance",
"text": [
"peripheral blood"
],
"offsets": [
[
153,
169
]
],
"normalized": []
},
{
"id": "PMID-1683740_T5",
"type": "Multi-tissue_structure",
"text": [
"bone marrow"
],
"offsets": [
[
267,
278
]
],
"normalized": []
},
{
"id": "PMID-1683740_T6",
"type": "Cell",
"text": [
"Lymphocyte"
],
"offsets": [
[
302,
312
]
],
"normalized": []
},
{
"id": "PMID-1683740_T7",
"type": "Cell",
"text": [
"T"
],
"offsets": [
[
340,
341
]
],
"normalized": []
},
{
"id": "PMID-1683740_T8",
"type": "Cell",
"text": [
"B-cells"
],
"offsets": [
[
346,
353
]
],
"normalized": []
},
{
"id": "PMID-1683740_T9",
"type": "Cell",
"text": [
"T-cells"
],
"offsets": [
[
433,
440
]
],
"normalized": []
},
{
"id": "PMID-1683740_T10",
"type": "Cell",
"text": [
"lymphocyte"
],
"offsets": [
[
529,
539
]
],
"normalized": []
},
{
"id": "PMID-1683740_T11",
"type": "Cell",
"text": [
"CD 4+ cells"
],
"offsets": [
[
568,
579
]
],
"normalized": []
},
{
"id": "PMID-1683740_T12",
"type": "Cell",
"text": [
"CD 8+ cells"
],
"offsets": [
[
613,
624
]
],
"normalized": []
},
{
"id": "PMID-1683740_T13",
"type": "Cell",
"text": [
"CD 4+ cells"
],
"offsets": [
[
687,
698
]
],
"normalized": []
},
{
"id": "PMID-1683740_T14",
"type": "Cell",
"text": [
"suppressor-inducer T-cells"
],
"offsets": [
[
730,
756
]
],
"normalized": []
},
{
"id": "PMID-1683740_T15",
"type": "Cell",
"text": [
"CD 8+ cells"
],
"offsets": [
[
792,
803
]
],
"normalized": []
},
{
"id": "PMID-1683740_T16",
"type": "Cell",
"text": [
"suppressor T-cells"
],
"offsets": [
[
841,
859
]
],
"normalized": []
},
{
"id": "PMID-1683740_T17",
"type": "Cell",
"text": [
"natural killer (NK) cells"
],
"offsets": [
[
882,
907
]
],
"normalized": []
},
{
"id": "PMID-1683740_T18",
"type": "Cell",
"text": [
"NK cells"
],
"offsets": [
[
923,
931
]
],
"normalized": []
},
{
"id": "PMID-1683740_T19",
"type": "Cell",
"text": [
"CD 16 -CD 57+ NK cells"
],
"offsets": [
[
1020,
1042
]
],
"normalized": []
},
{
"id": "PMID-1683740_T20",
"type": "Cell",
"text": [
"lymphocyte"
],
"offsets": [
[
1216,
1226
]
],
"normalized": []
},
{
"id": "PMID-1683740_T21",
"type": "Cell",
"text": [
"T-cells"
],
"offsets": [
[
1295,
1302
]
],
"normalized": []
},
{
"id": "PMID-1683740_T22",
"type": "Cell",
"text": [
"lymphocyte"
],
"offsets": [
[
1330,
1340
]
],
"normalized": []
},
{
"id": "PMID-1683740_T23",
"type": "Cell",
"text": [
"CD 4+ cells"
],
"offsets": [
[
1485,
1496
]
],
"normalized": []
},
{
"id": "PMID-1683740_T24",
"type": "Cell",
"text": [
"suppressor T-cells"
],
"offsets": [
[
1510,
1528
]
],
"normalized": []
},
{
"id": "PMID-1683740_T25",
"type": "Cell",
"text": [
"NK cells"
],
"offsets": [
[
1580,
1588
]
],
"normalized": []
},
{
"id": "PMID-1683740_T26",
"type": "Multi-tissue_structure",
"text": [
"graft"
],
"offsets": [
[
1140,
1145
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-1683740_R1",
"type": "frag",
"arg1_id": "PMID-1683740_T7",
"arg2_id": "PMID-1683740_T8",
"normalized": []
}
] |
PMID-3609047 | PMID-3609047 | [
{
"id": "PMID-3609047__text",
"type": "abstract",
"text": [
"Torsade de pointes during loading with amiodarone.\nTorsade de pointes represents a potential complication of chronic amiodarone therapy. Several reports have emphasized the need for a loading dose in order to achieve therapeutic blood levels rapidly. We report a case of torsade de pointes following a single oral dose of amiodarone (1400 mg or 30 mg kg-1) administered after short intravenous loading for prevention of paroxysmal atrial flutter. Torsades de pointes were preceded and associated with marked QT prolongation and bradycardia. This report suggests that careful monitoring of patients undergoing oral amiodarone loading is necessary.\n"
],
"offsets": [
[
0,
647
]
]
}
] | [
{
"id": "PMID-3609047_T1",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
229,
234
]
],
"normalized": []
},
{
"id": "PMID-3609047_T2",
"type": "Multi-tissue_structure",
"text": [
"intravenous"
],
"offsets": [
[
382,
393
]
],
"normalized": []
},
{
"id": "PMID-3609047_T3",
"type": "Multi-tissue_structure",
"text": [
"atrial"
],
"offsets": [
[
431,
437
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-19679742 | PMID-19679742 | [
{
"id": "PMID-19679742__text",
"type": "abstract",
"text": [
"Aging affects the cardiovascular responses to cold stress in humans.\nCardiovascular-related mortality peaks during cold winter months, particularly in older adults. Acute physiological responses, such as increases in blood pressure, in response to cold exposure may contribute to these associations. To determine whether the blood pressure-raising effect (pressor response) of non-internal body temperature-reducing cold stress is greater with age, we measured physiological responses to 20 min of superficial skin cooling, via water-perfused suit, in 12 younger [25 +/- 1 (SE) yr old] and 12 older (65 +/- 2 yr old) adults. We found that superficial skin cooling elicited an increase in blood pressure from resting levels (pressor response; P < 0.05) in younger and older adults. However, the magnitude of this pressor response (systolic and mean blood pressure) was more than twofold higher in older adults (P < 0.05 vs. younger adults). The magnitude of the pressor response was similar at peripheral (brachial) and central (estimated in the aorta) measurement sites. Regression analysis revealed that aortic pulse wave velocity, a measure of central arterial stiffness obtained before cooling, was the best predictor of the increased pressor response to superficial skin cooling in older adults, explaining approximately 63% of its variability. These results indicate that there is a greater pressor response to non-internal body temperature-reducing cold stress with age in humans that may be mediated by increased levels of central arterial stiffness.\n"
],
"offsets": [
[
0,
1558
]
]
}
] | [
{
"id": "PMID-19679742_T1",
"type": "Anatomical_system",
"text": [
"cardiovascular"
],
"offsets": [
[
18,
32
]
],
"normalized": []
},
{
"id": "PMID-19679742_T2",
"type": "Anatomical_system",
"text": [
"Cardiovascular"
],
"offsets": [
[
69,
83
]
],
"normalized": []
},
{
"id": "PMID-19679742_T3",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
217,
222
]
],
"normalized": []
},
{
"id": "PMID-19679742_T4",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
325,
330
]
],
"normalized": []
},
{
"id": "PMID-19679742_T5",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
510,
514
]
],
"normalized": []
},
{
"id": "PMID-19679742_T6",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
651,
655
]
],
"normalized": []
},
{
"id": "PMID-19679742_T7",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
688,
693
]
],
"normalized": []
},
{
"id": "PMID-19679742_T8",
"type": "Organism_subdivision",
"text": [
"brachial"
],
"offsets": [
[
1005,
1013
]
],
"normalized": []
},
{
"id": "PMID-19679742_T9",
"type": "Multi-tissue_structure",
"text": [
"aorta"
],
"offsets": [
[
1045,
1050
]
],
"normalized": []
},
{
"id": "PMID-19679742_T10",
"type": "Multi-tissue_structure",
"text": [
"aortic"
],
"offsets": [
[
1105,
1111
]
],
"normalized": []
},
{
"id": "PMID-19679742_T11",
"type": "Multi-tissue_structure",
"text": [
"arterial"
],
"offsets": [
[
1154,
1162
]
],
"normalized": []
},
{
"id": "PMID-19679742_T12",
"type": "Organ",
"text": [
"skin"
],
"offsets": [
[
1270,
1274
]
],
"normalized": []
},
{
"id": "PMID-19679742_T13",
"type": "Multi-tissue_structure",
"text": [
"arterial"
],
"offsets": [
[
1538,
1546
]
],
"normalized": []
},
{
"id": "PMID-19679742_T14",
"type": "Organism_substance",
"text": [
"blood"
],
"offsets": [
[
848,
853
]
],
"normalized": []
},
{
"id": "PMID-19679742_T15",
"type": "Organism_subdivision",
"text": [
"body"
],
"offsets": [
[
390,
394
]
],
"normalized": []
},
{
"id": "PMID-19679742_T16",
"type": "Organism_subdivision",
"text": [
"body"
],
"offsets": [
[
1429,
1433
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16850045 | PMID-16850045 | [
{
"id": "PMID-16850045__text",
"type": "abstract",
"text": [
"Fluoroscopically guided cervical prolotherapy for instability with blinded pre and post radiographic reading.\nBACKGROUND:\nSeveral authors have postulated that cervical instability is a major cause of traumatic spinal pain.\nOBJECTIVE:\nThe purpose of this prospective case series study (n = 6) was to determine if proliferant injections have an effect on cervical translation as measured by a blinded reader.\nDESIGN:\nThis study was a prospective case series. Study participants were selected from patients seen for the primary complaint of Motor Vehicle Collision related neck pain in a private sub-specialty pain clinic.\nMETHODS:\nFlexion and extension views were obtained by standard radiographs taken with a C-Arm fluoroscope under Valium sedation. Patients with more than 2.7 mm of absolute cervical translation and at least 50% reduction of cervical and referred pain with a two day rigid cervical immobilization test were admitted into the study. Participants underwent 3 prolotherapy injections at all sites that demonstrated translation. The difference in means between pre-test and post-test measurements (flexion translation, extension translation, and pain VAS scores) were assessed by a Wilcoxon signed ranks test (alpha = 0.05).\nRESULTS:\nThe mean post-test VAS score (M= 3.83, SD=2.3, t=2.889) was significantly less (p=0.04) than the mean pre-test VAS score (M=5.75, SD=1.94). The correlation between difference in mean extension at C2-3 and C5-6 and difference in mean extension was significant (rho=0.89, p=0.02 and rho=0.85, p=0.03 respectively). Difference in mean flexion at C3-4 and C4-5 was significantly correlated with difference in mean flexion (rho=0.88, p=0.02 and rho=0.941, p <0.01 respectively).\nCONCLUSIONS:\nThe results of this study demonstrate statistically significant correlations between proliferant injections, a reduction of both cervical flexion and extension translation, as well as a reduction in pain VAS score. Since patients with traumatic cervical instability have few viable treatment options other than surgical fusion, cervical proliferant injections under C-Arm fluoroscope may be a viable treatment option.\n"
],
"offsets": [
[
0,
2153
]
]
}
] | [
{
"id": "PMID-16850045_T1",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
24,
32
]
],
"normalized": []
},
{
"id": "PMID-16850045_T2",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
159,
167
]
],
"normalized": []
},
{
"id": "PMID-16850045_T3",
"type": "Organism_subdivision",
"text": [
"spinal"
],
"offsets": [
[
210,
216
]
],
"normalized": []
},
{
"id": "PMID-16850045_T4",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
353,
361
]
],
"normalized": []
},
{
"id": "PMID-16850045_T5",
"type": "Organism_subdivision",
"text": [
"neck"
],
"offsets": [
[
570,
574
]
],
"normalized": []
},
{
"id": "PMID-16850045_T6",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
792,
800
]
],
"normalized": []
},
{
"id": "PMID-16850045_T7",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
843,
851
]
],
"normalized": []
},
{
"id": "PMID-16850045_T8",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
891,
899
]
],
"normalized": []
},
{
"id": "PMID-16850045_T9",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
1864,
1872
]
],
"normalized": []
},
{
"id": "PMID-16850045_T10",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
1980,
1988
]
],
"normalized": []
},
{
"id": "PMID-16850045_T11",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
2063,
2071
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2959883-sec-06 | PMC-2959883-sec-06 | [
{
"id": "PMC-2959883-sec-06__text",
"type": "sec",
"text": [
"Data collection: CrystalClear (Rigaku/MSC, 2005 >); cell refinement: CrystalClear; data reduction: CrystalClear; program(s) used to solve structure: SHELXS97 (Sheldrick, 2008 >); program(s) used to refine structure: SHELXL97 (Sheldrick, 2008 >); molecular graphics: ORTEPII (Johnson, 1976 >); software used to prepare material for publication: SHELXL97.\n"
],
"offsets": [
[
0,
354
]
]
}
] | [
{
"id": "PMC-2959883-sec-06_T1",
"type": "Cell",
"text": [
"cell"
],
"offsets": [
[
52,
56
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2845033-sec-09 | PMC-2845033-sec-09 | [
{
"id": "PMC-2845033-sec-09__text",
"type": "sec",
"text": [
"Applying A1C cut offs to the AusDiab population (4.6% undiagnosed diabetes)\nApplying the same cut offs, a total 75.9% of the AusDiab population had diabetes ruled in or ruled out (Fig. 1B), while the remaining 24.1% had impaired A1C. From those with impaired A1C, 69.3% had abnormal glucose status. For diabetes, A1C at 5.5% provided moderate sensitivity (83.5%) but high NPV (99.0%), since diabetes prevalence was lower in the AusDiab than in the MP population. A1C at 7.0% gave 100% specificity and 100% PPV. By dropping the cut off to 6.5%, specificity remained 99.9%, with PPV near 100%.\n"
],
"offsets": [
[
0,
592
]
]
}
] | [] | [] | [] | [] |
PMID-15012488 | PMID-15012488 | [
{
"id": "PMID-15012488__text",
"type": "abstract",
"text": [
"Covariance structure analysis: statistical practice, theory, and directions.\nAlthough covariance structure analysis is used increasingly to analyze nonexperimental data, important statistical requirements for its proper use are frequently ignored. Valid conclusions about the adequacy of a model as an acceptable representation of data, which are based on goodness-of-fit test statistics and standard errors of parameter estimates, rely on the model estimation procedure being appropriate for the data. Using analogies to linear regression and anova, this review examines conditions under which conclusions drawn from various estimation methods will be correct and the consequences of ignoring these conditions. A distinction is made between estimation methods that are either correctly or incorrectly specified for the distribution of data being analyzed, and it is shown that valid conclusions are possible even under misspecification. A brief example illustrates the ideas. Internet access is given to a computer code for several methods that are not available in programs such as EQS or LISREL.\n"
],
"offsets": [
[
0,
1099
]
]
}
] | [] | [] | [] | [] |
PMID-3993849 | PMID-3993849 | [
{
"id": "PMID-3993849__text",
"type": "abstract",
"text": [
"Management of the tortuous internal carotid artery.\nThe tortuous internal carotid artery as the basis of cerebral vascular insufficiency is a controversial entity, as such lesions frequently occur without neurologic symptoms. However, some tortuous vessels are associated with significant carotid atherosclerotic disease requiring a specific surgical approach. This formed the basis of our report. Symptoms of cerebrovascular insufficiency in association with a tortuous internal carotid artery was encountered in 27 of 853 carotid endarterectomies over a 22 year period. Stenosis of hemodynamic significance was noted in nine patients and irregularities or ulceration were noted in the rest. With the standard technique of carotid endarterectomy, removal of plaque from a tortuous vessel leads to loss of the stenting effect provided by the plaque such that angulation occlusion is likely to occur. The optimal reconstruction in our experience is eversion endarterectomy by transection and lower reimplantation of the internal carotid artery on the common carotid artery. Our experience with 17 such procedures in 15 patients has been presented.\n"
],
"offsets": [
[
0,
1147
]
]
}
] | [
{
"id": "PMID-3993849_T1",
"type": "Multi-tissue_structure",
"text": [
"tortuous internal carotid artery"
],
"offsets": [
[
18,
50
]
],
"normalized": []
},
{
"id": "PMID-3993849_T2",
"type": "Multi-tissue_structure",
"text": [
"tortuous internal carotid artery"
],
"offsets": [
[
56,
88
]
],
"normalized": []
},
{
"id": "PMID-3993849_T3",
"type": "Multi-tissue_structure",
"text": [
"cerebral vascular"
],
"offsets": [
[
105,
122
]
],
"normalized": []
},
{
"id": "PMID-3993849_T4",
"type": "Pathological_formation",
"text": [
"lesions"
],
"offsets": [
[
172,
179
]
],
"normalized": []
},
{
"id": "PMID-3993849_T5",
"type": "Multi-tissue_structure",
"text": [
"tortuous vessels"
],
"offsets": [
[
240,
256
]
],
"normalized": []
},
{
"id": "PMID-3993849_T6",
"type": "Multi-tissue_structure",
"text": [
"cerebrovascular"
],
"offsets": [
[
410,
425
]
],
"normalized": []
},
{
"id": "PMID-3993849_T7",
"type": "Multi-tissue_structure",
"text": [
"tortuous internal carotid artery"
],
"offsets": [
[
462,
494
]
],
"normalized": []
},
{
"id": "PMID-3993849_T8",
"type": "Multi-tissue_structure",
"text": [
"carotid"
],
"offsets": [
[
524,
531
]
],
"normalized": []
},
{
"id": "PMID-3993849_T9",
"type": "Multi-tissue_structure",
"text": [
"carotid"
],
"offsets": [
[
724,
731
]
],
"normalized": []
},
{
"id": "PMID-3993849_T10",
"type": "Multi-tissue_structure",
"text": [
"tortuous vessel"
],
"offsets": [
[
773,
788
]
],
"normalized": []
},
{
"id": "PMID-3993849_T11",
"type": "Cell",
"text": [
"plaque"
],
"offsets": [
[
759,
765
]
],
"normalized": []
},
{
"id": "PMID-3993849_T12",
"type": "Cell",
"text": [
"plaque"
],
"offsets": [
[
842,
848
]
],
"normalized": []
},
{
"id": "PMID-3993849_T13",
"type": "Multi-tissue_structure",
"text": [
"internal carotid artery"
],
"offsets": [
[
1019,
1042
]
],
"normalized": []
},
{
"id": "PMID-3993849_T14",
"type": "Multi-tissue_structure",
"text": [
"common carotid artery"
],
"offsets": [
[
1050,
1071
]
],
"normalized": []
},
{
"id": "PMID-3993849_T15",
"type": "Multi-tissue_structure",
"text": [
"carotid"
],
"offsets": [
[
289,
296
]
],
"normalized": []
},
{
"id": "PMID-3993849_T16",
"type": "Anatomical_system",
"text": [
"neurologic"
],
"offsets": [
[
205,
215
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-8691230 | PMID-8691230 | [
{
"id": "PMID-8691230__text",
"type": "abstract",
"text": [
"Referral bias among health workers in studies using hospitalization as a proxy measure of the underlying incidence rate.\nContacts with health services like hospitals or general practitioners are usually the only available proxy measure of incidence of disease in studies based on secondary data and differential referrals or care-seeking behavior often bias such proxy measures. In former analyses based on the Occupational Hospitalization Register in Denmark assisting nurses had high Standardized Hospitalization Ratios for many diseases. It was, however, suspected that it fully or partly was due to a referral bias or self-selection to hospital treatment rather than exposures to occupational hazards. The aim of the present study is to evaluate the referral bias hypothesis by comparing hospitalization and mortality data for health workers for a disease category with a high mortality. Cohorts of all gainfully employed 20- to 59-year-old Danes were formed in order to compare Standardized Mortality Ratios and Standardized Hospitalization Ratios of ischemic heart disease (IHD) in occupational groups. The follow-up period was 10 years. For most of the investigated occupational groups a similar disease pattern was found whether hospitalization or death was used as the outcome measure. In \"nurse assistants\" a statistically significant higher risk was, however, found using hospitalization due to IHD as the end point rather than mortality. Additional analysis did not support the hypothesis that the finding could be explained by differentiated hospitalization due to social factors. The true incidence rates of the disease need not be equally well described by proxy measures such as hospitalization diagnosis or death diagnosis in all occupational groups. Differential access to medical treatment in some groups may lead to bias when hospital data are used as proxy measures for the underlying incidence rates.\n"
],
"offsets": [
[
0,
1923
]
]
}
] | [
{
"id": "PMID-8691230_T1",
"type": "Organ",
"text": [
"heart"
],
"offsets": [
[
1065,
1070
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-2861602-sec-09 | PMC-2861602-sec-09 | [
{
"id": "PMC-2861602-sec-09__text",
"type": "sec",
"text": [
"Discussion\nThis is the first study to employ such a large number of replicated samples in order to assess the bacterial communities of healthy and diseased corals, and the first culture-independent assessment of bacterial communities on Acroporid WS corals on the GBR. Despite the potential of not capturing rare or very low abundance bacterial ribotypes, the DGGE analysis used in this study indicated similar results of captured bacterial ribotypes and tentative bacterial species replacement in unhealthy corals to that of less replicated studies using other non-culture based techniques (e.g. [3], [54], [69]; Figure 4). The results from this research reinforce, with statistically relevant data, that corals harbour bacterial communities different to the water column [7], [9], [42], corroborate findings that corals associate only with certain specific bacterial groups, and that these coral-associated bacterial communities are 'host' species-specific [2]. The data presented here highlight a cluster of bacterial ribotypes frequently associated with corals, and the distribution of these bacterial ribotypes on healthy and diseased corals, which allows for further targeted research into a tentative link between these common coral associates and coral health. This study indicates that coral bacterial community assessments require a number of replicates per coral species and site to accurately describe the diversity present across the population and in order to draw inferences on health-related changes in the community composition. In addition, the comparisons of healthy and diseased Acropora hyacinthus samples showed that bacterial communities can change dramatically in diseased individuals. The DGGE profiles observed for corals displaying signs of White Syndrome comprised a range of bacterial ribotypes not generally found on healthy corals, including close relatives of bacteria previously found on Black Band Diseased corals. However the community profiles across the samples taken from diseased coral colonies were inconsistent and not indicative of a single bacterial causative agent.\n\n"
],
"offsets": [
[
0,
2111
]
]
}
] | [] | [] | [] | [] |
PMID-17523137 | PMID-17523137 | [
{
"id": "PMID-17523137__text",
"type": "abstract",
"text": [
"Characterization of transferrin glycoforms in human serum by CE-UV and CE-ESI-MS.\nHuman transferrin (Tf) is a model glycoprotein for congenital disorders of glycosylation (CDG) diagnosis. In the last few years, new CE-UV methods for intact Tf glycoforms analysis have been developed using nonvolatile BGEs and organic modifiers. However, the use of these BGEs does not allow the coupling of these procedures with electrospray MS (ESI-MS). In this study, a new CE-UV separation method of Tf glycoforms is developed, using a double-layer stable coating and a volatile BGE based on ammonium acetate. The separation method is optimized using standard Tf and their potential is demonstrated applying the method to the analysis of sera Tf from healthy individuals and CDG patients. The CE-UV separation method has been coupled to ESI-MS detection. Main parameters such as sheath liquid composition are optimized in order to obtain a good sensitivity. The CE-ESI-MS method has also been used in serum samples obtaining the separation of the different proteins present in serum and partial separation of Tf glycoforms. Different mass spectra and deconvoluted molecular masses were obtained for each sialoform, allowing unequivocal glycoform identification.\n"
],
"offsets": [
[
0,
1249
]
]
}
] | [
{
"id": "PMID-17523137_T1",
"type": "Organism_substance",
"text": [
"sera"
],
"offsets": [
[
725,
729
]
],
"normalized": []
},
{
"id": "PMID-17523137_T2",
"type": "Organism_substance",
"text": [
"serum samples"
],
"offsets": [
[
988,
1001
]
],
"normalized": []
},
{
"id": "PMID-17523137_T3",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
1064,
1069
]
],
"normalized": []
},
{
"id": "PMID-17523137_T4",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
52,
57
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-1698941-caption-09 | PMC-1698941-caption-09 | [
{
"id": "PMC-1698941-caption-09__text",
"type": "caption",
"text": [
"Comparison of the Predicted Irr Regulon and ICE Motifs with the Published Expression Microarray Data for Iron- and Irr-Affected Genes in Bradyrhizobium japonicum\n"
],
"offsets": [
[
0,
162
]
]
}
] | [] | [] | [] | [] |
PMC-2792620-sec-33 | PMC-2792620-sec-33 | [
{
"id": "PMC-2792620-sec-33__text",
"type": "sec",
"text": [
"Surgery\nTrabeculectomy should be considered in all patients, when the 'target IOP' is not achieved with glaucoma medications and if the expected rate of visual loss could affect the patient during their lifetime. In this procedure, an opening is made in the trabecular meshwork, so that aqueous humor can drain into the sclera.\nMany patients can discontinue glaucoma medications after surgery. Approximately one-third of the trabeculectomy patients develop cataract within five years. If trabeculectomy fails, another type of surgery places a drainage tube (Molteno tube) in the eye, between the cornea and iris, which exits at the junction of the cornea and sclera. Cyclodestructive procedures, which lower IOP by destroying the ciliary body, are typically reserved for eyes, which are refractory to all other forms of therapy. These procedures include cyclocryotherapy, cylcodiathermy and laser cyclophotocoagulation.[91-93]\n"
],
"offsets": [
[
0,
927
]
]
}
] | [
{
"id": "PMC-2792620-sec-33_T1",
"type": "Organism_substance",
"text": [
"humor"
],
"offsets": [
[
295,
300
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T2",
"type": "Multi-tissue_structure",
"text": [
"sclera"
],
"offsets": [
[
320,
326
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T3",
"type": "Organ",
"text": [
"eye"
],
"offsets": [
[
579,
582
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T4",
"type": "Multi-tissue_structure",
"text": [
"cornea"
],
"offsets": [
[
596,
602
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T5",
"type": "Multi-tissue_structure",
"text": [
"iris"
],
"offsets": [
[
607,
611
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T6",
"type": "Multi-tissue_structure",
"text": [
"cornea"
],
"offsets": [
[
648,
654
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T7",
"type": "Multi-tissue_structure",
"text": [
"sclera"
],
"offsets": [
[
659,
665
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T8",
"type": "Multi-tissue_structure",
"text": [
"ciliary body"
],
"offsets": [
[
730,
742
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T9",
"type": "Organ",
"text": [
"eyes"
],
"offsets": [
[
771,
775
]
],
"normalized": []
},
{
"id": "PMC-2792620-sec-33_T10",
"type": "Organ",
"text": [
"trabecular"
],
"offsets": [
[
258,
268
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-2028342 | PMID-2028342 | [
{
"id": "PMID-2028342__text",
"type": "abstract",
"text": [
"Posterior stabilization of the cervical spine with hook plates.\nHook-plate fixation is designed for posterior cervical stabilization from C2 to C7. Indications remain the same as for standard posterior fixations. The prime indications are discoligamentous injuries. The plates are hooked under the lower laminas and attached to the articular masses of the upper vertebra by oblique screws. An H-graft is placed between the spinous processes. The vertebrae are compressed together by the plates at three points, the facet joints, and graft. The resulting pre-stressed system is stable in all directions. A protocol for safe reduction of cervical dislocations is observed. Of 70 patients treated from 1979 to 1986, 51 were examined 12-54 months after surgery. All fusions consolidated. Two neurologic complications not attributable to the fixation occurred. Other major complications were not seen.\n"
],
"offsets": [
[
0,
897
]
]
}
] | [
{
"id": "PMID-2028342_T1",
"type": "Organism_subdivision",
"text": [
"cervical spine"
],
"offsets": [
[
31,
45
]
],
"normalized": []
},
{
"id": "PMID-2028342_T2",
"type": "Multi-tissue_structure",
"text": [
"lower laminas"
],
"offsets": [
[
298,
311
]
],
"normalized": []
},
{
"id": "PMID-2028342_T3",
"type": "Organ",
"text": [
"vertebra"
],
"offsets": [
[
362,
370
]
],
"normalized": []
},
{
"id": "PMID-2028342_T4",
"type": "Organ",
"text": [
"vertebrae"
],
"offsets": [
[
446,
455
]
],
"normalized": []
},
{
"id": "PMID-2028342_T5",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
636,
644
]
],
"normalized": []
},
{
"id": "PMID-2028342_T6",
"type": "Organism_subdivision",
"text": [
"cervical"
],
"offsets": [
[
110,
118
]
],
"normalized": []
},
{
"id": "PMID-2028342_T7",
"type": "Multi-tissue_structure",
"text": [
"articular masses"
],
"offsets": [
[
332,
348
]
],
"normalized": []
},
{
"id": "PMID-2028342_T8",
"type": "Anatomical_system",
"text": [
"neurologic"
],
"offsets": [
[
788,
798
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-2028342_R1",
"type": "Part-of",
"arg1_id": "PMID-2028342_T7",
"arg2_id": "PMID-2028342_T3",
"normalized": []
}
] |
PMC-1828719-sec-06 | PMC-1828719-sec-06 | [
{
"id": "PMC-1828719-sec-06__text",
"type": "sec",
"text": [
"Mass casualty estimation on a geographic basis\nThe Defense Threat Reduction Agency (DTRA) has expended considerable effort to develop models for calculating mass casualties from a nuclear detonation. In order to specifically evaluate urban medical systems vulnerability we are employing the PC based Consequence Assessment Tool Set (CATS) v6, with ESRI's ArcGIS9 [14], CATS/JACE (Joint Assessment of Catastrophic Events) v5 with ESRI's ArcView 3.3, Hazard Prediction and Assessment Capability (HPAC) V4.04SP3 [15], as well as custom GIS and database software applications. HPAC does excellent Chemical Biological and Nuclear (CBN) modeling, although output could provide more flexibility. Additionally, results can be exported to CATS for further analysis and display. All three programs can access the current weather data from both classified and unclassified weather servers. Examples of uses of CATS/HPAC are hurricane, tidal surge and earthquake damage, prediction of the results from nuclear, biological and chemical releases, assessment of persons and infrastructure affected and at risk (e.g. which hospitals and pharmacies are under a CBN plume and are thus out of commission), and mobilization of surviving and nearby infrastructure outside the plume that would be needed to address healthcare and other emergency response needs of the community.\nThese models have been, and continue to be, developed with a view to better estimating the impact of WMD weapons in an offensive setting. However, recent DTRA enhancements and our modifications have facilitated their use in helping estimate potential casualties from a WMD terrorist incident. One area of intense interest, and somewhat of a vacuum in public health planning, has been the utility of this approach in estimating medical care vulnerabilities in such an attack, and for the calculation of the distribution of surviving medical care resources. While much work has already occurred in estimating the impact of chemical weapons (due to the dual use in chemical spill management from transportation and industrial accidents), or in nuclear power plant accident management, much less research and development has gone into estimating the impact on our civilian population of a nuclear weapon detonation from a terrorist incident in a large urban area. The models already calculate such factors as the impact of blast, thermal effects and fallout, but results are often not available at the detail level needed for civil defense purposes, casualty management, and planning the use of scarce health resources in response to a nuclear weapon detonation. Furthermore, the models do not readily facilitate the calculation of injuries from multiple effects such as burns and blast with fallout or prompt radiation. The complexity of the urban three-dimensional landscape and its local impact on thermal, blast and radiation is also poorly understood. Additionally, given their traditional world-wide focus, and the increased sensitivity to providing information on the U.S.A. of use to terrorists, the models do not provide detailed or current data that exists for the United States that would help provide better casualty estimates and response. The models can be customized locally and data updated if the user has sufficient expertise. However, there is often a significant duplication of effort due to overlapping jurisdictions and the lack of data sharing due to security and other considerations.\nCATS and HPAC are also useful for creating realistic scenarios for training and planning before a disaster strikes, thus enabling responders to drill and exercise so they know roughly what to expect and how to react. Contingency plans can be created using comprehensive national and more detailed population and infrastructure data. Should disaster strike, the affected population and the impact on critical facilities can be quickly assessed, although efforts frequently need to be expended to ensure regional and local databases are current and useful.\n"
],
"offsets": [
[
0,
4017
]
]
}
] | [] | [] | [] | [] |
PMID-20157600 | PMID-20157600 | [
{
"id": "PMID-20157600__text",
"type": "abstract",
"text": [
"Further Characterization of Activin A-induced IgA Response in Murine B Lymphocytes.\nWe have recently shown that activin A, a member of TGF-beta superfamily, stimulates mouse B cells to express IgA isotype but other isotypes. In the present study, we further characterized effects of activin A on B cell growth and IgA expression. We found that activin A did not have effect on LPS-stimulated cell viability. In parallel, CFSE staining analysis revealed that activin A did not alter cell division. An increase of IgA secretion by activin A was completely abrogated by anti-activin A Ab but not by anti-TGFbeta1 Ab. In the same conditions, no other isotypes are significantly affected by each antibody treatment. Finally, activin A, as similar to TGF-beta1, increased IgA secretion by mesenteric lymph node cells. These results suggest that activin A can specifically stimulate IgA response, independent of TGF-beta in the gut.\n"
],
"offsets": [
[
0,
926
]
]
}
] | [
{
"id": "PMID-20157600_T1",
"type": "Cell",
"text": [
"B Lymphocytes"
],
"offsets": [
[
69,
82
]
],
"normalized": []
},
{
"id": "PMID-20157600_T2",
"type": "Cell",
"text": [
"B cells"
],
"offsets": [
[
174,
181
]
],
"normalized": []
},
{
"id": "PMID-20157600_T3",
"type": "Cell",
"text": [
"B cell"
],
"offsets": [
[
296,
302
]
],
"normalized": []
},
{
"id": "PMID-20157600_T4",
"type": "Cell",
"text": [
"cell"
],
"offsets": [
[
392,
396
]
],
"normalized": []
},
{
"id": "PMID-20157600_T5",
"type": "Cell",
"text": [
"cell"
],
"offsets": [
[
482,
486
]
],
"normalized": []
},
{
"id": "PMID-20157600_T6",
"type": "Cell",
"text": [
"lymph node cells"
],
"offsets": [
[
794,
810
]
],
"normalized": []
},
{
"id": "PMID-20157600_T7",
"type": "Organism_subdivision",
"text": [
"gut"
],
"offsets": [
[
921,
924
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-3266646-sec-09 | PMC-3266646-sec-09 | [
{
"id": "PMC-3266646-sec-09__text",
"type": "sec",
"text": [
"Origins of Acquired Antibiotic Resistance Mechanisms\nRecently, D'Costa et al. (2011) have reported a metagenomic analysis of the Beringian permafrost, which is 30,000 years old. They showed molecular evidences of the ancient origins of antibiotic resistances, detecting beta-lactamases genes, vanX-like, component of the vancomycin resistance operon, and tetM, coding for a protein protecting the ribosomal target from tetracycline. Sequence analysis revealed that the beta-lactamases genes recovered from the permafrost demonstrated an amino-acid homology (53-84%) to known beta-lactamases from beta-lactams producing Streptomyces. The tetM sequences revealed a high similarity to the genes coding for the ribosomal protection protein of actinomycetes. The vanX sequence showed a similarity to the vanX gene recovered in pathogenic vancomycin resistant enterococci (VRE) and to the vanX gene from Amycolatopsis orientalis. This environmental species, belonging to the actinobacteria phylum, is a natural producer of vancomycin, and very likely the progenitor of the van genes operons, responsible for resistance to vancomycin. The integration of the van operons on transposons and on conjugative plasmids has enhanced their spread (Courvalin, 2006). Reports of VRE in freshwater have been provided by several authors (Talebi et al., 2008; Lata et al., 2009; Luczkiewicz et al., 2010). Interestingly, Schwartz et al. (2003) detected vanA genes in the biofilm of drinking water supplies, in the absence of enterococci, demonstrating the lateral transfer of this gene. Notably, the progenitors of these resistance genes are soil bacteria thus most likely, a shuttle has been responsible for the introduction of these genes into the commensal bacterial community and afterward into the pathogenic species.\n\n"
],
"offsets": [
[
0,
1804
]
]
}
] | [
{
"id": "PMC-3266646-sec-09_T1",
"type": "Cellular_component",
"text": [
"ribosomal"
],
"offsets": [
[
397,
406
]
],
"normalized": []
},
{
"id": "PMC-3266646-sec-09_T2",
"type": "Cellular_component",
"text": [
"ribosomal"
],
"offsets": [
[
707,
716
]
],
"normalized": []
},
{
"id": "PMC-3266646-sec-09_T3",
"type": "Cellular_component",
"text": [
"conjugative plasmids"
],
"offsets": [
[
1185,
1205
]
],
"normalized": []
},
{
"id": "PMC-3266646-sec-09_T5",
"type": "Cell",
"text": [
"biofilm"
],
"offsets": [
[
1451,
1458
]
],
"normalized": []
}
] | [] | [] | [] |
PMC-194858-caption-04 | PMC-194858-caption-04 | [
{
"id": "PMC-194858-caption-04__text",
"type": "caption",
"text": [
"Extrapyramidal symptoms based on Extrapyramidal Symptoms Rating Scale\n"
],
"offsets": [
[
0,
70
]
]
}
] | [] | [] | [] | [] |
PMID-17607547 | PMID-17607547 | [
{
"id": "PMID-17607547__text",
"type": "abstract",
"text": [
"Selective activation of mast cells in rheumatoid synovial tissue results in production of TNF-alpha, IL-1beta and IL-1Ra.\nOBJECTIVES AND DESIGN:\nTo study the consequences of mast cell activation in human synovial tissue.\nMETHODS:\nSynovial tissue was obtained from 18 RA patients and mast cells was selectively activated in synovial tissue explant cultures. Expression of TNF-alpha, IL-1beta and IL-1Ra were determined and tissue distribution of IL-1beta was studied.\nRESULTS:\nCompared to untreated synovia, selective activation of synovial mast cells increased significantly the production of TNF-alpha (0.49 +/- 0.88 vs. 4.56 +/- 3.18 pg/mg wet tissue, p < 0.001) and IL-1beta (0.058 +/- 0.032 vs. 2.55 +/- 1.98 pg/mg wet tissue, p = 0.013). The expression of TNF-alpha and IL-1beta mRNA increased significantly (19-fold (p = 0.009) and 13-fold (p = 0.031), respectively). Mast cell activation induced IL-1beta expression in particular in nearby CD68 positive synovial macrophages. Secretion of IL-1Ra was also increased but to a lesser degree than that of IL-1beta.\nCONCLUSIONS:\nSynovial mast cells produce proinflammmatory cytokines and may thus contribute to the inflammation in RA.\n"
],
"offsets": [
[
0,
1187
]
]
}
] | [
{
"id": "PMID-17607547_T1",
"type": "Cell",
"text": [
"mast cells"
],
"offsets": [
[
24,
34
]
],
"normalized": []
},
{
"id": "PMID-17607547_T2",
"type": "Tissue",
"text": [
"rheumatoid synovial tissue"
],
"offsets": [
[
38,
64
]
],
"normalized": []
},
{
"id": "PMID-17607547_T3",
"type": "Cell",
"text": [
"mast cell"
],
"offsets": [
[
174,
183
]
],
"normalized": []
},
{
"id": "PMID-17607547_T4",
"type": "Tissue",
"text": [
"synovial tissue"
],
"offsets": [
[
204,
219
]
],
"normalized": []
},
{
"id": "PMID-17607547_T5",
"type": "Tissue",
"text": [
"Synovial tissue"
],
"offsets": [
[
230,
245
]
],
"normalized": []
},
{
"id": "PMID-17607547_T6",
"type": "Cell",
"text": [
"mast cells"
],
"offsets": [
[
283,
293
]
],
"normalized": []
},
{
"id": "PMID-17607547_T7",
"type": "Tissue",
"text": [
"synovial tissue"
],
"offsets": [
[
323,
338
]
],
"normalized": []
},
{
"id": "PMID-17607547_T8",
"type": "Tissue",
"text": [
"tissue"
],
"offsets": [
[
422,
428
]
],
"normalized": []
},
{
"id": "PMID-17607547_T9",
"type": "Tissue",
"text": [
"synovia"
],
"offsets": [
[
498,
505
]
],
"normalized": []
},
{
"id": "PMID-17607547_T10",
"type": "Cell",
"text": [
"synovial mast cells"
],
"offsets": [
[
531,
550
]
],
"normalized": []
},
{
"id": "PMID-17607547_T11",
"type": "Cell",
"text": [
"Mast cell"
],
"offsets": [
[
874,
883
]
],
"normalized": []
},
{
"id": "PMID-17607547_T12",
"type": "Cell",
"text": [
"CD68 positive synovial macrophages"
],
"offsets": [
[
947,
981
]
],
"normalized": []
},
{
"id": "PMID-17607547_T13",
"type": "Cell",
"text": [
"Synovial mast cells"
],
"offsets": [
[
1081,
1100
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-16927570 | PMID-16927570 | [
{
"id": "PMID-16927570__text",
"type": "abstract",
"text": [
"[The prevalence of ADHD and attention problems in preschool-aged children. A comparison of two diagnostic instruments].\nOBJECTIVES:\nIn order to analyse the prevalence of ADHD and attention problems in preschool-aged children, mothers were asked to rate their children using two measuring instruments.\nMETHODS:\nThe analysis is part of a prospective, randomised control study of N = 280 children aged three to six years, whose mothers rated them using the Child Behaviour Checklist/CBCL 1 1/2-5 and the Parent Rating Scale for Attention-Deficit Hyperactivity Disorder (ADHD).\nRESULTS:\nThe prevalence rates ranged from 2.7% to 9.9%. There was no significant gender effect in this age group.\nCONCLUSIONS:\nThe study delivers initial findings and provides support for decisions to implement in Germany new assessment methods for preschool-aged children with ADHD or hyperkinetic syndrome. Finally, the different rates of prevalence and the implications of the findings for epidemiology and the prevention of ADHD and attention problems among preschool-aged children are discussed.\n"
],
"offsets": [
[
0,
1075
]
]
}
] | [] | [] | [] | [] |
PMC-2949661-caption-02 | PMC-2949661-caption-02 | [
{
"id": "PMC-2949661-caption-02__text",
"type": "caption",
"text": [
"Summary of instrument characteristics\n"
],
"offsets": [
[
0,
38
]
]
}
] | [] | [] | [] | [] |
PMC-2946364-caption-05 | PMC-2946364-caption-05 | [
{
"id": "PMC-2946364-caption-05__text",
"type": "caption",
"text": [
"Effect of the deletion of IRE1alpha on the liver.\n(A) HE-stained sections of the liver tissue (scale bar: 50 mum). (B) Comparison of the serum AST and ALT levels between the IRE1alpha CKO mice and the control mice. Data are expressed as mean +/- S.E.M (n = 5). (C) Quantitative PCR analysis of lipid synthesis genes in the liver of mice fed normal or high-fructose feed. Columns indicate mean and error bars denote S.E.M (n = 3). All the data were obtained from 20 weeks old male mice.\n"
],
"offsets": [
[
0,
486
]
]
}
] | [
{
"id": "PMC-2946364-caption-05_T1",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
43,
48
]
],
"normalized": []
},
{
"id": "PMC-2946364-caption-05_T2",
"type": "Tissue",
"text": [
"liver tissue"
],
"offsets": [
[
81,
93
]
],
"normalized": []
},
{
"id": "PMC-2946364-caption-05_T3",
"type": "Tissue",
"text": [
"sections"
],
"offsets": [
[
65,
73
]
],
"normalized": []
},
{
"id": "PMC-2946364-caption-05_T4",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
137,
142
]
],
"normalized": []
},
{
"id": "PMC-2946364-caption-05_T5",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
323,
328
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMC-2946364-caption-05_R1",
"type": "Part-of",
"arg1_id": "PMC-2946364-caption-05_T3",
"arg2_id": "PMC-2946364-caption-05_T2",
"normalized": []
}
] |
PMC-2709655-sec-17 | PMC-2709655-sec-17 | [
{
"id": "PMC-2709655-sec-17__text",
"type": "sec",
"text": [
"Discussion\nBecause Netherton syndrome exhibits allergic phenotype, it is reasonable to speculate that SPINK5, which is mutated in Netherton syndrome, may act as a candidate gene for asthma and other allergic diseases [9]. An extensive search for single nucleotide polymorphisms in the SPINK5 led to the identification of a number of SNPs, including six nonsynonymous SNPs in coding region that might perturb its immune function. Subsequent genotyping of three nonsynonymous SNPs, A1103G, G1156A and G1258A in two independent panels of British families showed a significant association between SNP G1258A (Glu420Lys) and atopy, atopic dermatitis, elevated serum IgE levels and asthma [10]. This association was confirmed in a large German population and two Japanese populations [16-18]. Kato et al analyzed eight SNPs in exon 13 and 14 of the SPINK5 including G1258A (Glu420Lys), and found a positive association of seven SNPs with atopic dermatitis in a Japanese study sample using a case-control study design [16]. Nishio et al surveyed five of six previously reported nonsynonymous SPINK5 SNPs in Japanese atopic families identified through asthmatic children or subjects with atopic dermatitis and found that SPINK5 was associated with development of atopic dermatitis but not asthma [17]. Kabesch M et al. analyzed G1258A (Glu420Lys) in a German population of school children, and found its association with asthma as well as a concomitant occurrence of asthma and atopic dermatitis [18]. However, two subsequent studies failed to replicate the original SPINK5 findings for allergic diseases [19,20]. Folster-Holst et al genotyped four nonsynonymous SNPs (Asp106Asn, Asn368Ser, Asp386Asn, and Glu420Lys), and detected no association between SPINK5 and atopic dermatitis in populations of Northern German origin [20]. Jongepier H et al. failed to detect any association between SPINK5 and asthma, atopic phenotypes and atopic dermatitis in a Dutch population [19]. These discordant findings probably reflect different genetic and environmental backgrounds in various populations. To determine whether nonsynonymous SNPs of the SPINK5 are involved in the pathogenesis of asthma in the Chinese Han population, we performed a case-control study by genotyping four nonsynonymous SNPs in the SPINK5. We did not detect any significant association between these nonsynonymous SNPs and asthma in our Chinese samples. With our sample size, we expected a power of at least 80% in detecting an effect of OR >=1.3 for each of these SNPs. Therefore, our failure to detect an association for these 4 SNPs was not due to the sample size. These results suggest that the polymorphisms in the coding region of the SPINK5 are unlikely to contribute to asthma risk in the Chinese Han population. However, because our patients were ascertained for asthma, we could not exclude a role of the coding SNPs of the SPINK5 in atopic dermatitis in our population.\nThe variations in the regulatory sequences of genes may determine risks to common diseases by causing different levels of expression. Therefore, the identification and functional evaluation of polymorphisms in promoter region are of great value in understanding the genetic susceptibility to asthma. In order to determine the role of the SPINK5 promoter polymorphism in the pathogenesis of asthma, we genotyped a promoter polymorphism, -206G>A, in 422 asthma patients and 410 controls, and found a marginal association. The frequency of allele G was significantly higher in asthmatic patients than that in controls (p = 0.022). To confirm the association, additional 267 asthma patients and 301 controls newly recruited from the same hospital were genotyped, and the -206G>A polymorphism remained significantly associated with asthma (P = 0.001), even after Bonferroni correction(adjusted P = 0.01). To our knowledge, this is the first report of an association of -206G>A polymorphism with asthma. We further examined the potential functional role of this promoter polymorphism, and found that the G to A substitution at -206 generated a GATA-3 transcription factor binding site.\nMajor transcription factors controlling Th1 and Th2 development, such as T-box transcription factor and GATA3, are possibly involved in asthma and atopic diseases. GATA-3, a transcription factor specifically expressed in T helper 2 (Th2) cells, plays a critical role in the differentiation of Th2 cells from uncommitted CD4+ lymphocytes. In addition, GATA-3 is essential for the expression of the cytokines IL-4, IL-5 and IL-13 that mediate allergic inflammation [23]. Our luciferase reporter assay confirmed that SNP -206G>A is associated with the transcriptional activity of SPINK5. The G allele was associated with decreased transcriptional activity of the SPINK5. The mechanism by which the -206G>A SNP affects SPINK5 expression may be explained by the potential differential transcription factor binding of GATA binding factor, since -206G>A is located at the core sequence of GATA binding factor binding site. Electrophoretic mobility shift assay confirmed that the A to G substitution at -206 significantly reduced the binding efficiency of nuclear proteins to this element. Our data suggest that loss of GATA transcription factor regulation with the -206G may decrease the SPINK5 expression and thereby potentially perturb the immunosuppressive function of LEKTI.\n"
],
"offsets": [
[
0,
5392
]
]
}
] | [
{
"id": "PMC-2709655-sec-17_T1",
"type": "Cell",
"text": [
"T helper 2 (Th2) cells"
],
"offsets": [
[
4341,
4363
]
],
"normalized": []
},
{
"id": "PMC-2709655-sec-17_T2",
"type": "Cell",
"text": [
"Th2 cells"
],
"offsets": [
[
4413,
4422
]
],
"normalized": []
},
{
"id": "PMC-2709655-sec-17_T3",
"type": "Cell",
"text": [
"CD4+ lymphocytes"
],
"offsets": [
[
4440,
4456
]
],
"normalized": []
},
{
"id": "PMC-2709655-sec-17_T4",
"type": "Cellular_component",
"text": [
"nuclear"
],
"offsets": [
[
5168,
5175
]
],
"normalized": []
},
{
"id": "PMC-2709655-sec-17_T5",
"type": "Organism_substance",
"text": [
"serum"
],
"offsets": [
[
655,
660
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-6653557 | PMID-6653557 | [
{
"id": "PMID-6653557__text",
"type": "abstract",
"text": [
"Purification and characterization of various esterases from rat liver.\nThe major rat liver microsomal esterases acting on o-nitrophenylacetate with isoelectric points 5.0, 5.5, 6.1 and 6.4 were resolved by isoelectric focusing. Molecular weights were determined by sedimentation analysis in isokinetic gradients of sucrose and, after purification, in sodium dodecyl sulphate/polyacrylamide gel electrophoresis. Their subunit molecular weights were between 57 000 and 60 000. They behaved as monomers except the pI-6.1 enzyme which behaved as a trimer. Esterases of pI 5.0, pI 6.1 and pI 6.4 behaved like glycoproteins of the polymannose type in the presence of 125I-labelled concanavalin A. Preparations of the pI-5.0 enzyme contained two esterases of highly homologous structure. Antibodies directed against this preparation did not inhibit but precipitated pI-5.0 esterase activity quantitatively. They did not react with the pI-6.1 and pI-6.4 esterases but precipitated several nonimmunologically related esterases. Two of these enzymes were inducible by phenobarbital. Total activity was very low in 3-day-old animals. Individual esterase activities rose at different rates during development; the enzyme focusing near pI 5.0 was about three times more active in adult females than in males. All microsomal esterases are located on the luminal side of the endoplasmic reticulum.\n"
],
"offsets": [
[
0,
1383
]
]
}
] | [
{
"id": "PMID-6653557_T1",
"type": "Organ",
"text": [
"liver"
],
"offsets": [
[
64,
69
]
],
"normalized": []
},
{
"id": "PMID-6653557_T2",
"type": "Cellular_component",
"text": [
"liver microsomal"
],
"offsets": [
[
85,
101
]
],
"normalized": []
},
{
"id": "PMID-6653557_T3",
"type": "Cellular_component",
"text": [
"endoplasmic reticulum"
],
"offsets": [
[
1360,
1381
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-10744669 | PMID-10744669 | [
{
"id": "PMID-10744669__text",
"type": "abstract",
"text": [
"Genuine monovalent ligands of TrkA nerve growth factor receptors reveal a novel pharmacological mechanism of action.\nDeveloping small molecule agonistic ligands for tyrosine kinase receptors has been difficult, and it is generally thought that such ligands require bivalency. Moreover, multisubunit receptors are difficult to target, because each subunit contributes to ligand affinity, and each subunit may have distinct and sometimes opposing functions. Here, the nerve growth factor receptor subunits p75 and the tyrosine kinase TrkA were studied using artificial ligands that bind specifically to their extracellular domain. Bivalent TrkA ligands afford robust signals. However, genuine monomeric and monovalent TrkA ligands afford partial agonism, activate the tyrosine kinase activity, cause receptor internalization, and induce survival and differentiation in cell lines and primary neurons. Monomeric and monovalent TrkA ligands can synergize with ligands that bind the p75 subunit. However, the p75 ligands used in this study must be bivalent, and monovalent p75 ligands have no effect. These findings will be useful in designing and developing screens of small molecules selective for tyrosine kinase receptors and indicate that strategies for designing agonists of multisubunit receptors require consideration of the role of each subunit. Last, the strategy of using anti-receptor mAbs and small molecule hormone mimics as receptor ligands could be applied to the study of many other heteromeric cell surface receptors.\n"
],
"offsets": [
[
0,
1531
]
]
}
] | [
{
"id": "PMID-10744669_T3",
"type": "Cell",
"text": [
"cell lines"
],
"offsets": [
[
867,
877
]
],
"normalized": []
},
{
"id": "PMID-10744669_T4",
"type": "Cell",
"text": [
"neurons"
],
"offsets": [
[
890,
897
]
],
"normalized": []
},
{
"id": "PMID-10744669_T5",
"type": "Cellular_component",
"text": [
"cell surface"
],
"offsets": [
[
1507,
1519
]
],
"normalized": []
},
{
"id": "PMID-10744669_T6",
"type": "Immaterial_anatomical_entity",
"text": [
"extracellular"
],
"offsets": [
[
607,
620
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-21423801 | PMID-21423801 | [
{
"id": "PMID-21423801__text",
"type": "abstract",
"text": [
"Saliva proteins of vector Culicoides modify structure and infectivity of bluetongue virus particles.\nBluetongue virus (BTV) and epizootic haemorrhagic disease virus (EHDV) are related orbiviruses, transmitted between their ruminant hosts primarily by certain haematophagous midge vectors (Culicoides spp.). The larger of the BTV outer-capsid proteins, 'VP2', can be cleaved by proteases (including trypsin or chymotrypsin), forming infectious subviral particles (ISVP) which have enhanced infectivity for adult Culicoides, or KC cells (a cell-line derived from C. sonorensis). We demonstrate that VP2 present on purified virus particles from 3 different BTV strains can also be cleaved by treatment with saliva from adult Culicoides. The saliva proteins from C. sonorensis (a competent BTV vector), cleaved BTV-VP2 more efficiently than those from C. nubeculosus (a less competent/non-vector species). Electrophoresis and mass spectrometry identified a trypsin-like protease in C. sonorensis saliva, which was significantly reduced or absent from C. nubeculosus saliva. Incubating purified BTV-1 with C. sonorensis saliva proteins also increased their infectivity for KC cells ~10 fold, while infectivity for BHK cells was reduced by 2-6 fold. Treatment of an 'eastern' strain of EHDV-2 with saliva proteins of either C. sonorensis or C. nubeculosus cleaved VP2, but a 'western' strain of EHDV-2 remained unmodified. These results indicate that temperature, strain of virus and protein composition of Culicoides saliva (particularly its protease content which is dependent upon vector species), can all play a significant role in the efficiency of VP2 cleavage, influencing virus infectivity. Saliva of several other arthropod species has previously been shown to increase transmission, infectivity and virulence of certain arboviruses, by modulating and/or suppressing the mammalian immune response. The findings presented here, however, demonstrate a novel mechanism by which proteases in Culicoides saliva can also directly modify the orbivirus particle structure, leading to increased infectivity specifically for Culicoides cells and, in turn, efficiency of transmission to the insect vector.\n"
],
"offsets": [
[
0,
2198
]
]
}
] | [
{
"id": "PMID-21423801_T1",
"type": "Cell",
"text": [
"KC cells"
],
"offsets": [
[
526,
534
]
],
"normalized": []
},
{
"id": "PMID-21423801_T2",
"type": "Cell",
"text": [
"cell-line"
],
"offsets": [
[
538,
547
]
],
"normalized": []
},
{
"id": "PMID-21423801_T3",
"type": "Cell",
"text": [
"KC cells"
],
"offsets": [
[
1168,
1176
]
],
"normalized": []
},
{
"id": "PMID-21423801_T4",
"type": "Cell",
"text": [
"BHK cells"
],
"offsets": [
[
1209,
1218
]
],
"normalized": []
},
{
"id": "PMID-21423801_T5",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
2129,
2134
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-10357269 | PMID-10357269 | [
{
"id": "PMID-10357269__text",
"type": "abstract",
"text": [
"Enterococci at the crossroads of food safety?\nEnterococci are gram-positive bacteria and fit within the general definition of lactic acid bacteria. Modern classification techniques resulted in the transfer of some members of the genus Streptococcus, notably some of the Lancefield's group D streptococci, to the new genus Enterococcus. Enterococci can be used as indicators of faecal contamination. They have been implicated in outbreaks of foodborne illness, and they have been ascribed a beneficial or detrimental role in foods. In processed meats, enterococci may survive heat processing and cause spoilage, though in certain cheeses the growth of enterococci contributes to ripening and development of product flavour. Some enterococci of food origin produce bacteriocins that exert anti-Listeria activity. Enterococci are used as probiotics to improve the microbial balance of the intestine, or as a treatment for gastroenteritis in humans and animals. On the other hand, enterococci have become recognised as serious nosocomial pathogens causing bacteraemia, endocarditis, urinary tract and other infections. This is in part explained by the resistance of some of these bacteria to most antibiotics that are currently in use. Resistance is acquired by gene transfer systems, such as conjugative or nonconjugative plasmids or transposons. Virulence of enterococci is not well understood but adhesins, haemolysin, hyaluronidase, aggregation substance and gelatinase are putative virulence factors. It appears that foods could be a source of vancomycin-resistant enterococci. This review addresses the issue of the health risk of foods containing enterococci.\n"
],
"offsets": [
[
0,
1663
]
]
}
] | [
{
"id": "PMID-10357269_T1",
"type": "Organism_substance",
"text": [
"faecal"
],
"offsets": [
[
377,
383
]
],
"normalized": []
},
{
"id": "PMID-10357269_T2",
"type": "Organism_subdivision",
"text": [
"meats"
],
"offsets": [
[
544,
549
]
],
"normalized": []
},
{
"id": "PMID-10357269_T3",
"type": "Organ",
"text": [
"intestine"
],
"offsets": [
[
886,
895
]
],
"normalized": []
},
{
"id": "PMID-10357269_T4",
"type": "Multi-tissue_structure",
"text": [
"urinary tract"
],
"offsets": [
[
1079,
1092
]
],
"normalized": []
},
{
"id": "PMID-10357269_T5",
"type": "Cellular_component",
"text": [
"conjugative"
],
"offsets": [
[
1289,
1300
]
],
"normalized": []
},
{
"id": "PMID-10357269_T6",
"type": "Cellular_component",
"text": [
"nonconjugative plasmids"
],
"offsets": [
[
1304,
1327
]
],
"normalized": []
}
] | [] | [] | [
{
"id": "PMID-10357269_R1",
"type": "frag",
"arg1_id": "PMID-10357269_T5",
"arg2_id": "PMID-10357269_T6",
"normalized": []
}
] |
PMID-12748830 | PMID-12748830 | [
{
"id": "PMID-12748830__text",
"type": "abstract",
"text": [
"Impact of technology on the utilisation of positron emission tomography in lymphoma: current and future perspectives.\nPositron emission tomography (PET) has now gained a place in the management of patients with cancer, including those with Hodgkin's disease and non-Hodgkin's lymphoma. Restaging studies and those addressing the monitoring of response to treatment are especially in focus. Most of the knowledge gained has been achieved with dedicated BGO-based PET technology, but there are a number of developments that will impact on the use of this metabolic imaging technique in the investigation of patients with lymphoma. The challenges ahead are determined by the need for high-quality whole-body imaging associated with increased patient throughput and the need to investigate the role of new labelled ligands. The latter are likely to yield new insights into tumour cell characterisation, tumour behaviour and tumour outcome assessment. The study of new radiolabelled ligands will impose further demands for rapid dynamic data acquisition and accurate tracer quantification. Current and future developments in PET technology range from the use of new detector materials to different detector geometries and data acquisition modes. The search for alternatives to BGO scintillation materials for PET has led to the development of PET instruments utilising new crystals such as LSO and GSO. The use of these new detectors and the increased sensitivity achieved with 3D data acquisitions represent the most significant current developments in the field. With the increasing demands imposed on the clinical utilisation of PET, issues such as study cost and patient throughput will emerge as significant future factors. As a consequence, low-cost units are being offered by the manufacturers through the utilisation of gamma camera-based SPET systems for PET coincidence imaging. Unfortunately, clinical studies in lymphoma and other cancers have already demonstrated the limitations of this technology, with 20% of lesions <15 mm in size escaping detection. On the other hand, the recent development of combined PET/CT devices attempts to address the lack of anatomical information inherent with PET images, taking advantage of further improvement in patient throughput and hence cost-effectiveness. Preliminary studies using this multimodality imaging approach have already demonstrated the potential of the technique. Although the potential exists, certain technical issues with PET/CT require refinement of the methodology. Such issues include organ movement (such as respiratory motion), which strongly influences the image fusion of a rapidly acquired CT scan with the slower acquisition of a PET dataset, and the derivation of CT-based attenuation coefficients in the presence of contrast agents or metallic implants. The application of the technology for radiotherapy planning also poses a number of associated challenges. Finally, the development of dedicated PET systems based on planar detector arrangements with new detector components has the potential to improve clinical throughput by over 100%, but clinical trials using such systems have still to be carried out in order to establish the associated whole-body image quality.\n"
],
"offsets": [
[
0,
3246
]
]
}
] | [
{
"id": "PMID-12748830_T1",
"type": "Pathological_formation",
"text": [
"lymphoma"
],
"offsets": [
[
75,
83
]
],
"normalized": []
},
{
"id": "PMID-12748830_T2",
"type": "Pathological_formation",
"text": [
"cancer"
],
"offsets": [
[
211,
217
]
],
"normalized": []
},
{
"id": "PMID-12748830_T3",
"type": "Pathological_formation",
"text": [
"non-Hodgkin's lymphoma"
],
"offsets": [
[
262,
284
]
],
"normalized": []
},
{
"id": "PMID-12748830_T4",
"type": "Pathological_formation",
"text": [
"lymphoma"
],
"offsets": [
[
619,
627
]
],
"normalized": []
},
{
"id": "PMID-12748830_T5",
"type": "Cell",
"text": [
"tumour cell"
],
"offsets": [
[
869,
880
]
],
"normalized": []
},
{
"id": "PMID-12748830_T6",
"type": "Pathological_formation",
"text": [
"tumour"
],
"offsets": [
[
899,
905
]
],
"normalized": []
},
{
"id": "PMID-12748830_T7",
"type": "Pathological_formation",
"text": [
"tumour"
],
"offsets": [
[
920,
926
]
],
"normalized": []
},
{
"id": "PMID-12748830_T8",
"type": "Pathological_formation",
"text": [
"lymphoma"
],
"offsets": [
[
1919,
1927
]
],
"normalized": []
},
{
"id": "PMID-12748830_T9",
"type": "Pathological_formation",
"text": [
"cancers"
],
"offsets": [
[
1938,
1945
]
],
"normalized": []
},
{
"id": "PMID-12748830_T10",
"type": "Pathological_formation",
"text": [
"lesions"
],
"offsets": [
[
2020,
2027
]
],
"normalized": []
},
{
"id": "PMID-12748830_T12",
"type": "Organ",
"text": [
"organ"
],
"offsets": [
[
2552,
2557
]
],
"normalized": []
},
{
"id": "PMID-12748830_T13",
"type": "Organism_subdivision",
"text": [
"body"
],
"offsets": [
[
3226,
3230
]
],
"normalized": []
},
{
"id": "PMID-12748830_T14",
"type": "Anatomical_system",
"text": [
"respiratory"
],
"offsets": [
[
2576,
2587
]
],
"normalized": []
}
] | [] | [] | [] |
PMID-2539554 | PMID-2539554 | [
{
"id": "PMID-2539554__text",
"type": "abstract",
"text": [
"Type-A cholecystokinin receptors in CHP212 neuroblastoma cells: evidence for association with G protein and activation of phosphoinositide hydrolysis.\n125I-Bolton Hunter-cholecystokinin octapeptide (BH-CCK8) and (-)-[3H]L-364718 membrane binding assays were used to identify and characterize cholecystokinin (CCK) receptors in CHP212 human neuroblastoma cells. The ligand binding properties of CCK receptors in these cells are similar to those found in pancreas (CCK-A sites) and differ from the predominant type of CCK binding site found in brain (CCK-B sites). The specific binding of 125I-BH-CCK8 but not (-)-[3H]L-364718 was reduced by the metabolically stable GTP analog guanosine 5'-(beta-delta-imido)trisphosphate. A substantial difference in the Bmax for the radiolabeled agonist (125I-BH-CCK8) and antagonist [(-)-[3H]L-364718] was noted. These observations are consistent with CCK receptors existing in guanine nucleotide-binding protein-coupled and -uncoupled states. Similar to its action in pancreatic acinar cells, CCK8(S) stimulated the accumulation of [3H]inositol phosphates in cells prelabeled with [3H]myo-inositol (EC50 = 3.2 +/- 0.4 nM; maximum response = 4.5 +/- 0.4 x basal). The intrinsic activity of CCK analogues in stimulating phosphoinositide hydrolysis was substantially less than their reported intrinsic activity in stimulating phosphoinositide hydrolysis in pancreatic acinar cells. The CHP212 neuroblastoma cell may serve as a useful model for the recently reported CCK-A binding site found in the central nervous system.\n"
],
"offsets": [
[
0,
1555
]
]
}
] | [
{
"id": "PMID-2539554_T1",
"type": "Cell",
"text": [
"CHP212 neuroblastoma cells"
],
"offsets": [
[
36,
62
]
],
"normalized": []
},
{
"id": "PMID-2539554_T2",
"type": "Cellular_component",
"text": [
"membrane"
],
"offsets": [
[
229,
237
]
],
"normalized": []
},
{
"id": "PMID-2539554_T3",
"type": "Cell",
"text": [
"CHP212"
],
"offsets": [
[
327,
333
]
],
"normalized": []
},
{
"id": "PMID-2539554_T4",
"type": "Cell",
"text": [
"neuroblastoma cells"
],
"offsets": [
[
340,
359
]
],
"normalized": []
},
{
"id": "PMID-2539554_T5",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
417,
422
]
],
"normalized": []
},
{
"id": "PMID-2539554_T6",
"type": "Organ",
"text": [
"pancreas"
],
"offsets": [
[
453,
461
]
],
"normalized": []
},
{
"id": "PMID-2539554_T7",
"type": "Organ",
"text": [
"brain"
],
"offsets": [
[
542,
547
]
],
"normalized": []
},
{
"id": "PMID-2539554_T8",
"type": "Cell",
"text": [
"pancreatic acinar cells"
],
"offsets": [
[
1004,
1027
]
],
"normalized": []
},
{
"id": "PMID-2539554_T9",
"type": "Cell",
"text": [
"cells"
],
"offsets": [
[
1095,
1100
]
],
"normalized": []
},
{
"id": "PMID-2539554_T10",
"type": "Cell",
"text": [
"pancreatic acinar cells"
],
"offsets": [
[
1390,
1413
]
],
"normalized": []
},
{
"id": "PMID-2539554_T11",
"type": "Cell",
"text": [
"CHP212 neuroblastoma cell"
],
"offsets": [
[
1419,
1444
]
],
"normalized": []
},
{
"id": "PMID-2539554_T12",
"type": "Anatomical_system",
"text": [
"central nervous system"
],
"offsets": [
[
1531,
1553
]
],
"normalized": []
}
] | [] | [] | [] |
End of preview. Expand
in Dataset Viewer.
Dataset Card for AnEM
AnEM corpus is a domain- and species-independent resource manually annotated for anatomical entity mentions using a fine-grained classification system. The corpus consists of 500 documents (over 90,000 words) selected randomly from citation abstracts and full-text papers with the aim of making the corpus representative of the entire available biomedical scientific literature. The corpus annotation covers mentions of both healthy and pathological anatomical entities and contains over 3,000 annotated mentions.
Citation Information
@inproceedings{ohta-etal-2012-open,
author = {Ohta, Tomoko and Pyysalo, Sampo and Tsujii, Jun{'}ichi and Ananiadou, Sophia},
title = {Open-domain Anatomical Entity Mention Detection},
journal = {},
volume = {W12-43},
year = {2012},
url = {https://aclanthology.org/W12-4304},
doi = {},
biburl = {},
bibsource = {},
publisher = {Association for Computational Linguistics}
}
- Downloads last month
- 97