PubMed:2171704 JSONTXT

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    jnlpba-st-training

    {"project":"jnlpba-st-training","denotations":[{"id":"T1","span":{"begin":27,"end":61},"obj":"protein"},{"id":"T2","span":{"begin":65,"end":93},"obj":"cell_type"},{"id":"T3","span":{"begin":480,"end":483},"obj":"protein"},{"id":"T4","span":{"begin":503,"end":506},"obj":"protein"},{"id":"T5","span":{"begin":611,"end":614},"obj":"protein"},{"id":"T6","span":{"begin":618,"end":660},"obj":"cell_line"},{"id":"T7","span":{"begin":1039,"end":1042},"obj":"protein"},{"id":"T8","span":{"begin":1114,"end":1117},"obj":"protein"},{"id":"T9","span":{"begin":1240,"end":1243},"obj":"protein"}],"text":"Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation.\nAbnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH."}

    PubmedHPO

    {"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":183,"end":205},"obj":"HP_0000124"},{"id":"T2","span":{"begin":183,"end":197},"obj":"HP_0012210"},{"id":"T3","span":{"begin":183,"end":197},"obj":"HP_0000077"},{"id":"T4","span":{"begin":268,"end":276},"obj":"HP_0001417"},{"id":"T5","span":{"begin":277,"end":301},"obj":"HP_0004912"},{"id":"T6","span":{"begin":294,"end":301},"obj":"HP_0002748"},{"id":"T7","span":{"begin":386,"end":402},"obj":"HP_0002148"},{"id":"T8","span":{"begin":1268,"end":1284},"obj":"HP_0002148"}],"text":"Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation.\nAbnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH."}

    pubmed-sentences-benchmark

    {"project":"pubmed-sentences-benchmark","denotations":[{"id":"S1","span":{"begin":0,"end":182},"obj":"Sentence"},{"id":"S2","span":{"begin":183,"end":308},"obj":"Sentence"},{"id":"S3","span":{"begin":309,"end":409},"obj":"Sentence"},{"id":"S4","span":{"begin":410,"end":535},"obj":"Sentence"},{"id":"S5","span":{"begin":536,"end":682},"obj":"Sentence"},{"id":"S6","span":{"begin":683,"end":859},"obj":"Sentence"},{"id":"S7","span":{"begin":860,"end":985},"obj":"Sentence"},{"id":"S8","span":{"begin":986,"end":1096},"obj":"Sentence"},{"id":"S9","span":{"begin":1097,"end":1182},"obj":"Sentence"},{"id":"S10","span":{"begin":1183,"end":1337},"obj":"Sentence"}],"text":"Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation.\nAbnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH."}

    genia-medco-coref

    {"project":"genia-medco-coref","denotations":[{"id":"C1","span":{"begin":27,"end":61},"obj":"NP"},{"id":"C2","span":{"begin":111,"end":144},"obj":"NP"},{"id":"C3","span":{"begin":156,"end":181},"obj":"NP"},{"id":"C4","span":{"begin":268,"end":307},"obj":"NP"},{"id":"C5","span":{"begin":359,"end":362},"obj":"NP"},{"id":"C6","span":{"begin":439,"end":448},"obj":"NP"},{"id":"C7","span":{"begin":465,"end":468},"obj":"NP"},{"id":"C8","span":{"begin":469,"end":484},"obj":"NP"},{"id":"C9","span":{"begin":503,"end":506},"obj":"NP"},{"id":"C10","span":{"begin":531,"end":534},"obj":"NP"},{"id":"C11","span":{"begin":611,"end":614},"obj":"NP"},{"id":"C12","span":{"begin":683,"end":725},"obj":"NP"},{"id":"C13","span":{"begin":921,"end":956},"obj":"NP"},{"id":"C14","span":{"begin":1114,"end":1117},"obj":"NP"},{"id":"C15","span":{"begin":1144,"end":1169},"obj":"NP"},{"id":"C16","span":{"begin":1240,"end":1243},"obj":"NP"},{"id":"C17","span":{"begin":1333,"end":1336},"obj":"NP"}],"relations":[{"id":"R1","pred":"coref-ident","subj":"C4","obj":"C2"},{"id":"R2","pred":"coref-ident","subj":"C5","obj":"C4"},{"id":"R3","pred":"coref-pron","subj":"C7","obj":"C6"},{"id":"R4","pred":"coref-ident","subj":"C8","obj":"C1"},{"id":"R5","pred":"coref-ident","subj":"C9","obj":"C8"},{"id":"R6","pred":"coref-ident","subj":"C10","obj":"C5"},{"id":"R7","pred":"coref-ident","subj":"C11","obj":"C9"},{"id":"R8","pred":"coref-ident","subj":"C13","obj":"C12"},{"id":"R9","pred":"coref-ident","subj":"C14","obj":"C11"},{"id":"R10","pred":"coref-ident","subj":"C15","obj":"C3"},{"id":"R11","pred":"coref-ident","subj":"C16","obj":"C11"},{"id":"R12","pred":"coref-ident","subj":"C17","obj":"C10"}],"text":"Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation.\nAbnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH."}

    GENIAcorpus

    {"project":"GENIAcorpus","denotations":[{"id":"T1","span":{"begin":27,"end":61},"obj":"protein_family_or_group"},{"id":"T2","span":{"begin":65,"end":93},"obj":"cell_type"},{"id":"T3","span":{"begin":97,"end":105},"obj":"multi_cell"},{"id":"T4","span":{"begin":111,"end":144},"obj":"other_name"},{"id":"T5","span":{"begin":156,"end":181},"obj":"other_name"},{"id":"T6","span":{"begin":183,"end":225},"obj":"other_name"},{"id":"T7","span":{"begin":250,"end":264},"obj":"other_name"},{"id":"T8","span":{"begin":268,"end":301},"obj":"other_name"},{"id":"T9","span":{"begin":303,"end":306},"obj":"other_name"},{"id":"T10","span":{"begin":336,"end":345},"obj":"lipid"},{"id":"T11","span":{"begin":359,"end":362},"obj":"other_name"},{"id":"T12","span":{"begin":386,"end":402},"obj":"other_name"},{"id":"T13","span":{"begin":439,"end":448},"obj":"lipid"},{"id":"T14","span":{"begin":480,"end":483},"obj":"protein_family_or_group"},{"id":"T15","span":{"begin":486,"end":499},"obj":"other_name"},{"id":"T16","span":{"begin":503,"end":506},"obj":"protein_family_or_group"},{"id":"T17","span":{"begin":531,"end":534},"obj":"other_name"},{"id":"T18","span":{"begin":611,"end":614},"obj":"protein_family_or_group"},{"id":"T19","span":{"begin":618,"end":631},"obj":"cell_line"},{"id":"T20","span":{"begin":632,"end":660},"obj":"cell_type"},{"id":"T21","span":{"begin":669,"end":672},"obj":"other_name"},{"id":"T22","span":{"begin":673,"end":681},"obj":"multi_cell"},{"id":"T23","span":{"begin":683,"end":691},"obj":"multi_cell"},{"id":"T24","span":{"begin":700,"end":725},"obj":"other_name"},{"id":"T25","span":{"begin":753,"end":766},"obj":"multi_cell"},{"id":"T26","span":{"begin":828,"end":843},"obj":"multi_cell"},{"id":"T27","span":{"begin":925,"end":947},"obj":"multi_cell"},{"id":"T28","span":{"begin":948,"end":956},"obj":"multi_cell"},{"id":"T29","span":{"begin":976,"end":984},"obj":"multi_cell"},{"id":"T30","span":{"begin":1039,"end":1042},"obj":"protein_family_or_group"},{"id":"T31","span":{"begin":1061,"end":1076},"obj":"atom"},{"id":"T32","span":{"begin":1104,"end":1112},"obj":"multi_cell"},{"id":"T33","span":{"begin":1114,"end":1117},"obj":"protein_family_or_group"},{"id":"T34","span":{"begin":1144,"end":1169},"obj":"other_name"},{"id":"T35","span":{"begin":1223,"end":1236},"obj":"other_name"},{"id":"T36","span":{"begin":1240,"end":1243},"obj":"protein_family_or_group"},{"id":"T37","span":{"begin":1268,"end":1284},"obj":"other_name"},{"id":"T38","span":{"begin":1309,"end":1318},"obj":"lipid"},{"id":"T39","span":{"begin":1333,"end":1336},"obj":"other_name"}],"text":"Decreased concentration of 1,25-dihydroxyvitamin D3 receptors in peripheral mononuclear cells of patients with X-linked hypophosphatemic rickets: effect of phosphate supplementation.\nAbnormal renal tubular phosphate transport is considered to be the primary defect in X-linked hypophosphatemic rickets (XLH). However, the resistance to vitamin D treatment in XLH cannot be explained by hypophosphatemia alone. Since most of the actions of vitamin D are mediated by its receptors (VDR), abnormalities of VDR have been postulated in XLH. In order to investigate this possibility, we measured the concentration of VDR in PHA-activated peripheral mononuclear cells from 10 XLH patients. Patients without phosphate supplementation showed significantly lower concentration (21.7 +/- 5.1 fmol/mg protein, mean +/- SEM) compared to the normal controls (60.7 +/- 4.0). On the contrary, there was no significant difference between the phosphate-supplemented patients (58.3 +/- 2.7) and controls. There was a significant positive correlation between VDR concentration and serum phosphate (P less than 0.05). In two patients, VDR was increased after daily phosphate supplementation was started. These results indicate that a decreased concentration of VDR secondary to persistent hypophosphatemia is one of the causes of vitamin D resistance in XLH."}