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1200
1200
These results indicate that polymorphisms in the @GENE$ gene are associated with susceptibility to @DISEASE$ due to Japanese cedar pollen, but the functional relationship still needs clarification.
[ "1" ]
1201
1201
The eNOS G894T or @GENE$ 894TT genotypes in combination with the MTHFR 677TT or ACE D/D genotype increases the risk of @DISEASE$.
[ "1" ]
1202
1202
These findings suggest a possible role for @GENE$ and other MHC genes in the @DISEASE$ of psoriasis.
[ "0" ]
1203
1203
These results suggest that the @GENE$ N367T and UGT2B17 null polymorphisms may modify the risk of @DISEASE$, particularly among men with a family history of the disease.
[ "1" ]
1204
1204
These data together with recent functional data on the direct effect of leptin on blood pressure suggest that the @GENE$ gene and its product, leptin, are an attractive target for studies on the mechanisms of hypertension and for the development of methods for the prediction, prevention, and therapy for @DISEASE$.
[ "1" ]
1205
1205
Although an increasing number of studies report an association between the @GENE$ G1385A variant and @DISEASE$ risk; this variant does not appear to be implicated in the development of breast cancer.
[ "0" ]
1206
1206
The presence of the C34T @DISEASE$ in @GENE$ gene appears to be protective against acute heart failure in cardiac donors.
[ "0" ]
1207
1207
In summary, our data suggest that common alleles at the @GENE$ locus modulate @DISEASE$ and metabolic variables in humans.
[ "0" ]
1208
1208
These results suggest that mutations in the HNF-1beta gene derived from a limited number of @DISEASE$ are not a major cause of common forms of @GENE$ 2 diabetes, even in the genetically homogeneous Japanese population.
[ "0" ]
1209
1209
Statistically insignificant association of @GENE$ gene polymorphism with @DISEASE$ was observed in studied group of patients.
[ "1" ]
1210
1210
The Leu544Ile polymorphism of the @GENE$ gene is associated with cholesterol levels in boys with GH @DISEASE$.
[ "0" ]
1211
1211
Identification of @GENE$ mutations in 12.2% of patients with adult alcoholic and idiopathic chronic pancreatitis suggests an important role for SPINK1 as a predisposing factor in adult @DISEASE$.
[ "1" ]
1212
1212
@GENE$ may be a risk factor for the development of @DISEASE$ and its association with emphysema may be stronger in smokers.
[ "0" ]
1213
1213
These results indicate that the T allele and TT genotype at CD14/-159 are risk factors for @GENE$ in @DISEASE$, and that the development of CAL in KD may be related to the magnitude of CD14 toll-like receptor response.
[ "0" ]
1214
1214
These results suggest that the hometown and socio-economic status are important environmental factors for gastric @DISEASE$, and @GENE$ polymorphic types could be associated with familial gastric carcinoma.
[ "0" ]
1215
1215
These data support the hypothesis that @GENE$ may mediate not only @DISEASE$, but may also modulate more common age-related disorders and, perhaps, a basic aging process.
[ "0" ]
1216
1216
An @GENE$ polymorphism in the promoter region may modulate the @DISEASE$ of cigarette smoking on pulmonary function in long-term cigarette smokers.
[ "0" ]
1217
1217
Our study suggests that there is a minor association between @GENE$-K and early-onset @DISEASE$, especially in the presence of the APOE-epsilon 4 allele.
[ "1" ]
1218
1218
The T-485A and the @GENE$-241-240TT may be functional polymorphisms, and the A-485 allele and TT-241-240/Pro2 haplotype are possible protective factors for the development of @DISEASE$.
[ "0" ]
1219
1219
The association between the @GENE$ C677T and SHMT ( 1 ) C1420T polymorphisms and the risk of ESCC and @DISEASE$ was demonstrated.
[ "0" ]
1220
1220
VDR overexpression in @DISEASE$ is independently associated with PIK3CA and @GENE$ mutations.
[ "1" ]
1221
1221
No evidence was found that @GENE$ mutations underlie human congenital structural @DISEASE$.
[ "0" ]
1222
1222
the @DISEASE$ polymorphism is associated with @GENE$, inflammatory disease behavior, and primary sclerosing cholangitis in Hungarian patients.
[ "0" ]
1223
1223
C allele homozygosity in position 786 of the @GENE$ promoter seems to be an independent risk factor for the development of moderate to severe ICA @DISEASE$, especially ulcerative lesions.
[ "0" ]
1224
1224
No @DISEASE$ causing mutations were identified in the @GENE$ gene in this cohort, indicating that mutations in this gene are unlikely to be responsible for HCM.
[ "0" ]
1225
1225
Our findings suggest that G-33A @DISEASE$ reduces the @GENE$ promoter activity and is associated with carotid atherosclerosis in younger subjects.
[ "0" ]
1226
1226
The current findings indicate that the @GENE$ H161R variant influences the risk of @DISEASE$ and is a natural IL-17F antagonist, suggesting a potential role for IL-17F in the etiology of asthma.
[ "1" ]
1227
1227
The @GENE$ gene 4a/b polymorphism was not associated with the extent of coronary atherosclerosis, but the a-allele of the variant seems to protect to some degree against the development of @DISEASE$.
[ "1" ]
1228
1228
The present study shows that R219K polymorphism of ABCA1 gene and G > C polymorphism in intron 7 of @GENE$ gene act cumulatively and synergistically in determining the risk of premature @DISEASE$.
[ "1" ]
1229
1229
Our results suggest that mutation of the @GENE$ gene is unlikely to play an important role in the mechanism of resistance to paclitaxel in @DISEASE$.
[ "1" ]
1230
1230
The data indicate that genetic variations of the heat @DISEASE$ proteins @GENE$ and HSPA1L may contribute to clinical outcome after severe injury.
[ "0" ]
1231
1231
These results suggest that -344T/C polymorphism of @GENE$ gene may be associated with @DISEASE$ in the Han nationality in Shandong province.
[ "0" ]
1232
1232
In spite of a relatively small sample size, the presence of the met-@GENE$ allele was found associated with a reduced volume of the hippocampal formation in healthy volunteers and may represent a vulnerability factor for the development of @DISEASE$ processes associated with the dysfunction of this brain region.
[ "0" ]
1233
1233
Common polymorphisms on @GENE$ and CYP3A5 genes do not modify the risk of developing @DISEASE$ in Western Europe.
[ "0" ]
1234
1234
We find no evidence to support an association between @GENE$ genotype and either the diagnosis of @DISEASE$ itself or progression of the disease.
[ "1" ]
1235
1235
A positive correlation was found between LRP gene polymorphism and AD, but not between @GENE$ gene polymorphism and AD in Chinese @DISEASE$ cases.
[ "1" ]
1236
1236
These results could implicate a functional role for the @GENE$ promoter polymorphism in the enhanced risk to develop @DISEASE$.
[ "1" ]
1237
1237
The results indicate that polymorphisms in the novel splice variant are not associated with @DISEASE$, but are in @GENE$ with other polymorphisms in OPRM1.
[ "0" ]
1238
1238
These data indicate that a single haplotype, X+Del, within the apo B gene exerts an @GENE$ on lipid metabolism and may contribute to the susceptibility to development of @DISEASE$ in males from a population of Brazilians.
[ "0" ]
1239
1239
@GENE$ gene -572G allele may be a genetic susceptibility factor to @DISEASE$ attack of Chinese Hans population, and related to the high expression of IL6.
[ "1" ]
1240
1240
Pending confirmation in prospective studies, the @GENE$ genotype of the MspI polymorphism of the Apo @DISEASE$ gene, within the Apo A-I/C-III/A-IV cluster, seems to be a risk factor for Type 2 diabetes mellitus.
[ "0" ]
1241
1241
These results indicate that @GENE$ G(-273)C has a significant effect on the HDL-C level in the general Japanese population, but not on the incidence of @DISEASE$.
[ "0" ]
1242
1242
@GENE$ has a role in the @DISEASE$ of MDD.
[ "0" ]
1243
1243
it is likely that PPARalpha gene does not have a major role in diabetes and CHD in our populations, although we can not exclude a minor contribution of the @GENE$ gene to the risk of @DISEASE$ associated with Type 2 diabetes through a modulation of atherogenic plasma lipids.
[ "1" ]
1244
1244
The association of variants in @GENE$ with @DISEASE$ and type 2 diabetes-related phenotypes and the differential expression of IRS1 in adipocytes and skeletal muscle suggest a role of this gene in the pathogenesis of type 2 diabetes in Pima Indians.
[ "1" ]
1245
1245
The association of variants in IRS1 with @DISEASE$ and type 2 diabetes-related phenotypes and the differential expression of @GENE$ in adipocytes and skeletal muscle suggest a role of this gene in the pathogenesis of type 2 diabetes in Pima Indians.
[ "1" ]
1246
1246
@GENE$ exon 11 @DISEASE$ is an independent adverse prognostic factor in patients with GIST.
[ "0" ]
1247
1247
Our results showed that polymorphisms of @GENE$ promoter may affect, at least in part, the outcomes of @DISEASE$ infection.
[ "0" ]
1248
1248
These findings suggest that genetic polymorphisms in @GENE$, IL-10 and TNFalpha may play important roles in developing @DISEASE$ in the Chinese population.
[ "1" ]
1249
1249
Our analysis of the entire coding region and three parts of the promoter of the MMP2 gene failed to show an association between genetic polymorphisms and AAA, suggesting that variations in the @GENE$ gene do not contribute to the development of @DISEASE$.
[ "1" ]
1250
1250
Our results suggest that @GENE$ promoter polymorphisms are associated with age at diagnosis of type 2 diabetes and early-onset @DISEASE$ in the Korean population.
[ "1" ]
1251
1251
In summary, our results show that @DISEASE$ is a complex disease which is not only caused by mutations in SLC7A9 and SLC3A1, but also influenced by other modifying factors such as variants in @GENE$.
[ "1" ]
1252
1252
In this population, there was an association between the homozygous @DISEASE$ form of @GENE$ (742G-->A) polymorphism and increased risk for placental abruption.
[ "0" ]
1253
1253
Lack of strong association suggests that the polymorphic TTTA short tandem repeat of @GENE$ gene may have not a functional effect on the enzyme's activity and thus its role in the development of @DISEASE$ remains unclear.
[ "1" ]
1254
1254
We conclude that activating mutations of the @GENE$ gene are not a major contributor to the development of @DISEASE$ in these data.
[ "1" ]
1255
1255
Although based on a limited number of patients, our work suggests that individuals who are NOS3-CC + @GENE$-DD are at a higher risk for early @DISEASE$, probably as a consequence of increased endothelial dysfunction.
[ "1" ]
1256
1256
Our results support the hypothesis that a genetic polymorphism in the @GENE$ gene may be associated with increased @DISEASE$ risk.
[ "1" ]
1257
1257
This study suggests that the @GENE$/W genotype of the MGMT gene may contribute to the de novo occurrence of @DISEASE$.
[ "0" ]
1258
1258
These data together with recent functional data on the direct effect of leptin on blood pressure suggest that the @GENE$ gene and its product, leptin, are an attractive target for studies on the mechanisms of @DISEASE$ and for the development of methods for the prediction, prevention, and therapy for hypertension.
[ "1" ]
1259
1259
We conclude from our data that @GENE$ might play a role in the genetic predisposition to @DISEASE$ and that these effects are different or even opposite to the effects on severe RSV diseases.
[ "0" ]
1260
1260
The @GENE$ intron 2 polymorphism may not be associated with the risk of @DISEASE$, but AA genotype or A allele of ABCA1 gene may have a protective effect for AD in Han Chinese.
[ "0" ]
1261
1261
The de novo origin of an RP1 (Arg677ter) mutation in a patient with simplex RP suggests that this common autosomal dominant @DISEASE$ mutation can arise independently in the population and supports the hypothesis of a mutational hotspot in the @GENE$ gene.
[ "1" ]
1262
1262
it is possible that common variants in the ATM and @GENE$ genes, in interaction with oestrogen-related exposures, are involved in @DISEASE$ aetiology.
[ "1" ]
1263
1263
Our data suggest that @GENE$ -1306 C-->T polymorphism may be associated with colorectal cancer development and @DISEASE$ in the Chinese population.
[ "0" ]
1264
1264
The results showed that the triplet repeat polymorphism in the promoter region of the @GENE$ gene was not likely to be involved in the pathogenesis or in the psychotic symptoms of @DISEASE$.
[ "1" ]
1265
1265
These results indicate that the genotypic profile of @GENE$ affects susceptibility to thyroid @DISEASE$, and that allelic loss of this gene is involved in thyroid carcinogenesis.
[ "0" ]
1266
1266
Our data do not support a role for the @GENE$ gene as genetic risk factor for @DISEASE$.
[ "1" ]
1267
1267
The results suggest that the 3 bp I/D polymorphism of the @GENE$ gene may be weakly associated with the susceptibility of @DISEASE$ in a Japanese population.
[ "1" ]
1268
1268
These data, therefore, suggest that the @GENE$ promoter polymorphisms C-482T and T-455C are associated with the @DISEASE$.
[ "0" ]
1269
1269
@GENE$ genotype modifies the association between alcohol @DISEASE$ and diabetes.
[ "0" ]
1270
1270
These data indicate that @GENE$ variants may predispose to a range of @DISEASE$ types of low malignant potential, but not to aggressive cancers.
[ "0" ]
1271
1271
Polymorphisms in the @GENE$ promoter region and TNF-receptor genes are not associated with the development of @DISEASE$.
[ "1" ]
1272
1272
The identical @GENE$ @DISEASE$ can be associated with both mild and severe forms of dilated cardiomyopathy.
[ "0" ]
1273
1273
@GENE$ N34S @DISEASE$ enhances the susceptibility of AP.
[ "0" ]
1274
1274
our data suggest that individuals provided with @GENE$*4 and NAT1*10 are at a significantly lower risk for @DISEASE$, particularly when exposed to environmental risk factors.
[ "1" ]
1275
1275
We found no evidence for a significant independent role for the CCR2 and @GENE$ variants in the susceptibility to or severity of @DISEASE$.
[ "1" ]
1276
1276
Our findings indicate that @GENE$ gene may be a candidate susceptibility gene for schizophrenia in Chinese Han population, and also provide further support for the potential importance of NMDAR-mediated glutamatergic @DISEASE$ in the etiology of schizophrenia.
[ "0" ]
1277
1277
This large-scale collaborative analysis demonstrates that @GENE$ REP1 allele-length variability is associated with an increased risk of @DISEASE$.
[ "1" ]
1278
1278
We conclude that sequence variation in the BACE1 or @GENE$ gene is not a significant risk factor for @DISEASE$; however, a combination of a specific BACE1 allele and APOE epsilon 4 may increase the risk for Alzheimer disease over and above that attributed to APOE epsilon 4 alone.
[ "1" ]
1279
1279
two common variant alleles of the MLH1 and @GENE$ genes make a substantial contribution to @DISEASE$ incidence in Ontario.
[ "1" ]
1280
1280
These results suggest that polymorphisms of @GENE$ are related to the development of polysubstance use in Japanese patients with MAP @DISEASE$.
[ "0" ]
1281
1281
We speculate that @GENE$ may interact with dopaminergic @DISEASE$ and dopamine receptor stimulation in the frontostriatal circuitry, with subsequent consequences on cognition in Parkinson's disease.
[ "0" ]
1282
1282
These findings provide initial support for genotype-specific phenotypes for @GENE$ in autism based on ratings from the @DISEASE$ Diagnostic Interview-Revised and Autism Diagnostic Observation Schedule.
[ "1" ]
1283
1283
The data suggest that the polymorphism in exon 10 of the XRCC1 gene may be associated with resistance to oxaliplatin/5-@GENE$ chemotherapy in advanced @DISEASE$.
[ "0" ]
1284
1284
The results supported our previous data, and suggest the possible involvement of the -333G>T and the -286A>G polymorphisms in the promoter region of the @GENE$ gene in the predisposition to @DISEASE$.
[ "1" ]
1285
1285
Longer microsatellites in the promoter of @GENE$ are associated to the exudative form of AMD and to body mass index, a well-known risk factor for the @DISEASE$.
[ "0" ]
1286
1286
Thus, in a random adult population with invasive @DISEASE$, @GENE$ does not seem to play a role in the pathophysiology, in contrast to earlier observations in patients with other concomitant immune abnormalities.
[ "0" ]
1287
1287
@GENE$ polymorphism A38G does not influence the predisposition to @DISEASE$ in this sample.
[ "1" ]
1288
1288
These data provide evidence that the rs2267668 A/G SNP in @GENE$ and the Gly482Ser SNP in PPARGC1A have both independent and additive effects on the effectiveness of aerobic exercise training to increase aerobic physical fitness and @DISEASE$.
[ "0" ]
1289
1289
Epistatic interaction between allelic variants of @GENE$ and IL12Bpro exert a significant influence on the clinical outcome of @DISEASE$-1 infection.
[ "1" ]
1290
1290
CTLA-4 49 @GENE$ is protective from @DISEASE$, whereas, CTLA-4 49 G allele (both as homozygotes and as heterozygotes ) confers an increased risk of diabetes mellitus.
[ "0" ]
1291
1291
@GENE$ might not play a major role in the susceptibility of @DISEASE$ in Japanese population.
[ "1" ]
1292
1292
We conclude that the described DMB polymorphisms are not associated with IDDM susceptibility and @GENE$ genotyping is unlikely to improve the assessment of genetic risk for @DISEASE$.
[ "1" ]
1293
1293
the @GENE$ promoter polymorphism was found to have an influence on PAI-1 levels in @DISEASE$ patients and on the risk of venous thrombosis in subjects with other genetic thrombophilic defects.
[ "0" ]
1294
1294
We cannot find support for the involvement of variation in @GENE$ in susceptibility to @DISEASE$, but the role of this and other genes from the phosphoinositol signalling pathway in predicting response to lithium treatment merits further investigation.
[ "1" ]
1295
1295
In conclusion, our results do not support an association between CT60A/G polymorphism and susceptibility to @DISEASE$ in the Spanish population, although the contribution of other positions located within the 3' region of the @GENE$ gene to RA susceptibility cannot be discarded.
[ "1" ]
1296
1296
We concluded that at least one susceptibility locus for @DISEASE$ is probably located within or nearby @GENE$ in the Japanese population.
[ "1" ]
1297
1297
Homozygosity for the @GENE$ 1186C variant is a @DISEASE$ risk factor for MI especially in older women.
[ "0" ]
1298
1298
while mitochondrial @DISEASE$ may be one of the most common medical conditions associated with autism, variation at the @GENE$ gene does not explain the high frequency of mitochondrial dysfunction markers and is not associated with autism in this sample of autistic patients.
[ "0" ]
1299
1299
Our results indicate that genetic variants in @GENE$, independent of @DISEASE$ treatment, are determinants of FEV1 in both adults and children with asthma, and suggest that STAT3 may participate in inflammatory pathways that have an impact on level of lung function.
[ "1" ]