| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-132 |
Sentence |
denotes |
Autosomal dominant hypophosphatemic rickets in an 85 year old woman: characterization of her disease from infancy through adulthood. |
| TextSentencer_T2 |
133-144 |
Sentence |
denotes |
BACKGROUND: |
| TextSentencer_T3 |
145-428 |
Sentence |
denotes |
Autosomal dominant hypophosphatemic rickets (ADHR) is a rare genetic disorder of phosphate homeostasis characterized, when severely expressed, by osteomalacia, suppressed levels of calcitriol, and renal phosphate wasting due to elevated levels of fibroblast growth factor 23 (FGF23). |
| TextSentencer_T4 |
429-544 |
Sentence |
denotes |
The disease is caused by heterozygous FGF23 mutations at the RXXR site that prevent cleavage of the intact hormone. |
| TextSentencer_T5 |
545-556 |
Sentence |
denotes |
OBJECTIVES: |
| TextSentencer_T6 |
557-696 |
Sentence |
denotes |
An FGF23 mutation was identified in the proband an 85-year-old woman with elevated FGF23 levels, and her clinical course was characterized. |
| TextSentencer_T7 |
697-763 |
Sentence |
denotes |
Medical records revealed she was treated for rickets as an infant. |
| TextSentencer_T8 |
764-890 |
Sentence |
denotes |
She was then asymptomatic until soon after her 4th pregnancy, when she suffered incapacitating bone pain and weakness, age 37. |
| TextSentencer_T9 |
891-930 |
Sentence |
denotes |
Symptoms remitted with brief treatment. |
| TextSentencer_T10 |
931-939 |
Sentence |
denotes |
RESULTS: |
| TextSentencer_T11 |
940-1057 |
Sentence |
denotes |
The proband and one son, but not other family members, were found to be heterozygous for the R176Q mutation in FGF23. |
| TextSentencer_T12 |
1058-1204 |
Sentence |
denotes |
Expression of this germ line mutation was strikingly different in both individuals in terms of skeletal health, FGF23 levels and disease activity. |
| TextSentencer_T13 |
1205-1217 |
Sentence |
denotes |
CONCLUSIONS: |
| TextSentencer_T14 |
1218-1419 |
Sentence |
denotes |
The identified FGF23 mutation in two members of this family raises questions about molecular mechanisms that have led to intermittent increases in FGF23 synthesis and secretion, and disease expression. |
| T1 |
0-132 |
Sentence |
denotes |
Autosomal dominant hypophosphatemic rickets in an 85 year old woman: characterization of her disease from infancy through adulthood. |
| T2 |
133-144 |
Sentence |
denotes |
BACKGROUND: |
| T3 |
145-428 |
Sentence |
denotes |
Autosomal dominant hypophosphatemic rickets (ADHR) is a rare genetic disorder of phosphate homeostasis characterized, when severely expressed, by osteomalacia, suppressed levels of calcitriol, and renal phosphate wasting due to elevated levels of fibroblast growth factor 23 (FGF23). |
| T4 |
429-544 |
Sentence |
denotes |
The disease is caused by heterozygous FGF23 mutations at the RXXR site that prevent cleavage of the intact hormone. |
| T5 |
545-556 |
Sentence |
denotes |
OBJECTIVES: |
| T6 |
557-696 |
Sentence |
denotes |
An FGF23 mutation was identified in the proband an 85-year-old woman with elevated FGF23 levels, and her clinical course was characterized. |
| T7 |
697-763 |
Sentence |
denotes |
Medical records revealed she was treated for rickets as an infant. |
| T8 |
764-890 |
Sentence |
denotes |
She was then asymptomatic until soon after her 4th pregnancy, when she suffered incapacitating bone pain and weakness, age 37. |
| T9 |
891-930 |
Sentence |
denotes |
Symptoms remitted with brief treatment. |
| T10 |
931-939 |
Sentence |
denotes |
RESULTS: |
| T11 |
940-1057 |
Sentence |
denotes |
The proband and one son, but not other family members, were found to be heterozygous for the R176Q mutation in FGF23. |
| T12 |
1058-1204 |
Sentence |
denotes |
Expression of this germ line mutation was strikingly different in both individuals in terms of skeletal health, FGF23 levels and disease activity. |
| T13 |
1205-1217 |
Sentence |
denotes |
CONCLUSIONS: |
| T14 |
1218-1419 |
Sentence |
denotes |
The identified FGF23 mutation in two members of this family raises questions about molecular mechanisms that have led to intermittent increases in FGF23 synthesis and secretion, and disease expression. |