| Id |
Subject |
Object |
Predicate |
Lexical cue |
| TextSentencer_T1 |
0-134 |
Sentence |
denotes |
Peroxisomal proliferator activated receptor-gamma deficiency in a Canadian kindred with familial partial lipodystrophy type 3 (FPLD3). |
| T1 |
0-134 |
Sentence |
denotes |
Peroxisomal proliferator activated receptor-gamma deficiency in a Canadian kindred with familial partial lipodystrophy type 3 (FPLD3). |
| TextSentencer_T2 |
135-146 |
Sentence |
denotes |
BACKGROUND: |
| T2 |
135-146 |
Sentence |
denotes |
BACKGROUND: |
| TextSentencer_T3 |
147-351 |
Sentence |
denotes |
Familial partial lipodystrophy (Dunnigan) type 3 (FPLD3, Mendelian Inheritance in Man [MIM] 604367) results from heterozygous mutations in PPARG encoding peroxisomal proliferator-activated receptor-gamma. |
| T3 |
147-351 |
Sentence |
denotes |
Familial partial lipodystrophy (Dunnigan) type 3 (FPLD3, Mendelian Inheritance in Man [MIM] 604367) results from heterozygous mutations in PPARG encoding peroxisomal proliferator-activated receptor-gamma. |
| TextSentencer_T4 |
352-448 |
Sentence |
denotes |
Both dominant-negative and haploinsufficiency mechanisms have been suggested for this condition. |
| T4 |
352-448 |
Sentence |
denotes |
Both dominant-negative and haploinsufficiency mechanisms have been suggested for this condition. |
| TextSentencer_T5 |
449-457 |
Sentence |
denotes |
METHODS: |
| T5 |
449-457 |
Sentence |
denotes |
METHODS: |
| TextSentencer_T6 |
458-620 |
Sentence |
denotes |
We present a Canadian FPLD3 kindred with an affected mother who had loss of fat on arms and legs, but no increase in facial, neck, suprascapular or abdominal fat. |
| T6 |
458-620 |
Sentence |
denotes |
We present a Canadian FPLD3 kindred with an affected mother who had loss of fat on arms and legs, but no increase in facial, neck, suprascapular or abdominal fat. |
| TextSentencer_T7 |
621-884 |
Sentence |
denotes |
She had profound insulin resistance, diabetes, severe hypertriglyceridemia and relapsing pancreatitis, while her pre-pubescent daughter had normal fat distribution but elevated plasma triglycerides and C-peptide and depressed high-density lipoprotein cholesterol. |
| T7 |
621-884 |
Sentence |
denotes |
She had profound insulin resistance, diabetes, severe hypertriglyceridemia and relapsing pancreatitis, while her pre-pubescent daughter had normal fat distribution but elevated plasma triglycerides and C-peptide and depressed high-density lipoprotein cholesterol. |
| TextSentencer_T8 |
885-893 |
Sentence |
denotes |
RESULTS: |
| T8 |
885-893 |
Sentence |
denotes |
RESULTS: |
| TextSentencer_T9 |
894-1104 |
Sentence |
denotes |
The mother and daughter were each heterozygous for PPARG nonsense mutation Y355X, whose protein product in vitro was transcriptionally inactive with no dominant-negative activity against the wild-type receptor. |
| T9 |
894-1104 |
Sentence |
denotes |
The mother and daughter were each heterozygous for PPARG nonsense mutation Y355X, whose protein product in vitro was transcriptionally inactive with no dominant-negative activity against the wild-type receptor. |
| TextSentencer_T10 |
1105-1169 |
Sentence |
denotes |
In addition the mutant protein appeared to be markedly unstable. |
| T10 |
1105-1169 |
Sentence |
denotes |
In addition the mutant protein appeared to be markedly unstable. |
| TextSentencer_T11 |
1170-1181 |
Sentence |
denotes |
CONCLUSION: |
| T11 |
1170-1181 |
Sentence |
denotes |
CONCLUSION: |
| TextSentencer_T12 |
1182-1481 |
Sentence |
denotes |
Taken together with previous studies of human PPARG mutations, these findings suggest that PPAR-gamma deficiency due either to haploinsufficiency or to substantial activity loss due to dominant negative interference of the normal allele product's function can each contribute to the FPLD3 phenotype. |
| T12 |
1182-1481 |
Sentence |
denotes |
Taken together with previous studies of human PPARG mutations, these findings suggest that PPAR-gamma deficiency due either to haploinsufficiency or to substantial activity loss due to dominant negative interference of the normal allele product's function can each contribute to the FPLD3 phenotype. |