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800
The present study revealed an association between carrier state of Q allele of @GENE$ gene and @DISEASE$ as well as synergistic effects between genotype and some conventional risk factors, mainly smoking and elevated level of total cholesterol.
[ "1" ]
801
801
Our results suggest that APOE and @GENE$ genotypes may be independent risk factors for late-onset @DISEASE$, but the ACE association needs to be confirmed in independent samples in which the time and extent of vascular cofactors can be assessed.
[ "1" ]
802
802
polymorphisms in the @GENE$ gene analyzed here are not associated with @DISEASE$ in a Japanese population.
[ "1" ]
803
803
These data suggest that a @DISEASE$ in the @GENE$ gene promoter region, or a mutation in linkage disequilibrium with the promoter SNP, may be involved in the pathogenesis of chromosome 22-linked SZ.
[ "0" ]
804
804
@GENE$ insertion/@DISEASE$ polymorphism may determine rHuEPO responsiveness in CAPD patients and should be considered in relative rHuEPO resistance.
[ "0" ]
805
805
it is unlikely that @GENE$ E1317Q is associated with a clinically meaningful risk of @DISEASE$.
[ "1" ]
806
806
our study suggests that @GENE$ gene variants have no major influence on suicidal behavior but may modulate @DISEASE$ features.
[ "0" ]
807
807
The genetic information about @GENE$ from this study would be useful for further genetic study of obesity, @DISEASE$, and other metabolic diseases.
[ "0" ]
808
808
Together, @DISEASE$ is not associated with a promoter polymorphism in the @GENE$ gene nor with the production of IL-12p70 by LPS-stimulated blood cells.
[ "1" ]
809
809
These results suggest that @GENE$ polymorphisms/haplotypes may contribute to genetic susceptibility for @DISEASE$.
[ "1" ]
810
810
Our results suggest that S100B could be a susceptible gene for @DISEASE$ and provide indirect evidence for the @GENE$/SD hypothesis.
[ "0" ]
811
811
Although it has been hypothesized that the T(-295)C promoter polymorphism may be associated with increased @GENE$ gene expression, it is not associated with @DISEASE$, disease severity or atopy in this Australian population.
[ "0" ]
812
812
We conclude that functional @GENE$-uVNTR alleles may act as a genetic modifier of the severity of @DISEASE$ in males.
[ "1" ]
813
813
Our results suggest that deletion polymorphism of the @GENE$ gene is not associated with the pathogenesis of @DISEASE$ in Taiwanese.
[ "1" ]
814
814
The @DISEASE$ of phenotypic differences in normal tension glaucoma patients with and without the @GENE$ polymorphisms IVS 8 +4 C/T; +32 T/C suggest that these OPA1 polymorphisms do not underlie any major phenotypic diversity in these patients.
[ "0" ]
815
815
@GENE$ TaqIB polymorphism is significantly associated with the presence of @DISEASE$ in the context of micro- or macroalbuminuria, elevated C-reactive protein, renal dysfunction, and ischemic heart disease.
[ "1" ]
816
816
It is unlikely that the promoter polymorphisms -359T/C and -303A/G of the catalytic subunit @GENE$ gene of human PI 3-kinase have a major impact on insulin secretion, @DISEASE$, or the risk of type 2 diabetes in Finnish subjects.
[ "0" ]
817
817
The above results suggest that the Msp I polymorphisms of @GENE$ itself might not be associated with idiopathic early-onset @DISEASE$.
[ "1" ]
818
818
The results suggest that the familial @DISEASE$ is associated to the @GENE$ gene.
[ "0" ]
819
819
Persons who are homozygous for the @GENE$ +874A allele may have a higher risk of contracting @DISEASE$.
[ "1" ]
820
820
In the present case-control study, we found no evidence of an association between the Glu298Asp variant of the @GENE$ gene and @DISEASE$/MI among Taiwanese.
[ "1" ]
821
821
Our results suggest that the presence of these two @GENE$ polymorphisms may be a marker of genetic susceptibility to @DISEASE$.
[ "0" ]
822
822
These results suggested that @GENE$ polymorphism is associated with the impairment of aortic and carotid distensibility in patients with @DISEASE$.
[ "1" ]
823
823
@GENE$-antitrypsin @DISEASE$ is not related to the pathogenesis of idiopathic or hereditary CP.
[ "0" ]
824
824
No evidence for association of @GENE$ with @DISEASE$ was detected using family or case-control methods.
[ "1" ]
825
825
The results indicate that specific polymorphisms in the @GENE$, ESR1, and ESR2 genes may play a role in progression of BBD to @DISEASE$ among Caucasian women.
[ "1" ]
826
826
In conclusion, our study suggests a potential role of the K121Q polymorphism or derived @GENE$ haplotypes in increased susceptibility to @DISEASE$ and early impairment of glucose and insulin metabolism in children.
[ "0" ]
827
827
Our results collectively suggest that SNPs and haplotypes of the @GENE$ promoter region are associated with @DISEASE$ risk in the Korean population.
[ "1" ]
828
828
The lack of statistically significant difference between G/G frequencies in both groups of patients may suggest that @GENE$ G/G genotype is not a risk factor for @DISEASE$.
[ "1" ]
829
829
No association was seen between @GENE$ genotype and either @DISEASE$ or therapeutic response, suggesting that the benefits of treatment most likely overshadow the salutary effects of the V64I polymorphism.
[ "0" ]
830
830
The ChAT @GENE$ is a novel genetic risk factor @DISEASE$, and the SSVS is a useful approach for analyzing association with multiple candidate genes simultaneously.
[ "0" ]
831
831
Although the studied polymorphisms have been previously reported to constitute risk factors for the disease, we found no association between LTC4S -444 A/C, @GENE$ -176/-147, and ALOX5AP -169/-146 polymorphisms and @DISEASE$.
[ "1" ]
832
832
Although @GENE$ genetic variability is not related to the development of @DISEASE$, identification of variant haplotypes may, after larger prospective studies have been performed, provide clinicians with a tool for methadone dosage individualization.
[ "0" ]
833
833
In conclusion, we described a significant association between @GENE$ gene polymorphisms and @DISEASE$, suggesting a new genetic susceptibility factor for hyperinsulinemia, insulin resistance, and type 2 diabetes.
[ "1" ]
834
834
our study does not support the notion that @GENE$ and HTR1A gene variants are major contributors to @DISEASE$-, anger-, or aggression-related behaviors in our sample.
[ "0" ]
835
835
The increased allele sharing in the @GENE$ gene region on 19p13 is consistent with an important involvement of this region in migraine, especially @DISEASE$.
[ "0" ]
836
836
In our population, the +1073 C/T @GENE$ polymorphism exhibited a significant association with Alzheimer's disease, further supporting the role of OLR1 as a candidate risk gene for sporadic @DISEASE$.
[ "1" ]
837
837
Our data suggest that @GENE$ Q192R polymorphism was not independently associated with MI but further increased the risk of @DISEASE$ among the subjects with DM, obesity, or both, the conditions associated with high oxidative stress.
[ "1" ]
838
838
Both analyses support (@GENE$.046 for the proposed test, p = 0.028 for the case-control analysis) an association of the homozygous GSTM1 @DISEASE$ genotype with autism.
[ "0" ]
839
839
Mutations of the @GENE$ and of the GPR54 gene are rare in IHH and should be investigated especially in cases with autosomal recessive @DISEASE$.
[ "0" ]
840
840
The @GENE$-159 and -550 polymorphisms might not play a major role in the @DISEASE$ of food allergy in Japanese children.
[ "0" ]
841
841
These data point to a role of the @GENE$ haplotype in @DISEASE$ and raise the possibility of relative thienopyridine resistance in carriers of the P2Y12 H2 haplotype.
[ "0" ]
842
842
Since none of the remaining DRB1*04 subtypes was associated with type 1 DM, our study may present another piece of evidence that the DRB1*0401 and @GENE$*0404 alleles do not modify @DISEASE$ risk generally in European populations.
[ "1" ]
843
843
We conclude that carriers of a @GENE$ 936T-allele are at decreased risk for @DISEASE$, this, however, requiring further confirmation in a larger study.
[ "1" ]
844
844
The results from this study indicate that polymorphisms in LRP and @GENE$ are not associated with increased risk for @DISEASE$ in Northern Ireland.
[ "1" ]
845
845
In conclusion, this study revealed a strong association between P-selectin gene polymorphisms and serum @GENE$ levels and a complex age-dependent relation between soluble P-selectin levels and @DISEASE$, which suggests that this molecule might have different roles in the atherothrombotic process.
[ "1" ]
846
846
Results from this study suggest that rs4680 in the COMT gene and rs4646903 in the @GENE$ gene may be genetic markers for @DISEASE$ prognosis in Chinese women.
[ "1" ]
847
847
Our results show that besides @DISEASE$ stage, lymph node status, and tumor grade, the @GENE$ T393C status is a novel independent host factor for disease progression in patients with clear cell renal cell carcinoma and provides further evidence for the T393C polymorphism as a general prognostic tumor marker.
[ "0" ]
848
848
Although @GENE$ genotype was not reliably associated with @DISEASE$ lib drinking behavior, the results suggest that individuals with the long-long (LL) genotype may develop acute tolerance to alcohol effects more rapidly than heterozygotes or individuals homozygous for the short SERT allele.
[ "0" ]
849
849
These results indicate that elevated baseline @GENE$ levels and PPARA gene intron 7 G/G genotype were associated with TG reduction > 30% after fenofibrate treatment in patients with @DISEASE$.
[ "0" ]
850
850
Our data indicate that the X-chromosomal located +1675 G/A-polymorphism of the @GENE$-R gene is associated with LV structure in young male humans with early structural changes of the heart due to @DISEASE$.
[ "1" ]
851
851
We conclude that @GENE$ gene polymorphism is not associated with development of @DISEASE$.
[ "1" ]
852
852
The observation that CYP3A4 and CYP3A43 were associated with @DISEASE$, are not in linkage equilibrium, and are both involved in testosterone metabolism, suggest that both @GENE$*1B and CYP3A43*3 may influence the probability of having prostate cancer and disease severity.
[ "1" ]
853
853
We conclude that the @GENE$ V600E @DISEASE$ in microsatellite-stable colon cancer is associated with a significantly poorer survival in stages 2 to 4 colon cancer but has no effect on the excellent prognosis of microsatellite-unstable tumors.
[ "0" ]
854
854
These results indicate that the @GENE$ variant haplotype is functionally significant in patients with sepsis, being associated with increased nuclear @DISEASE$ of NF-kappaB, more severe organ dysfunction, and higher mortality.
[ "0" ]
855
855
Our findings suggest that the A-G polymorphism of @GENE$ may confer susceptibility to @DISEASE$ behavior in MD patients.
[ "1" ]
856
856
@GENE$ G38A polymorphism had no association with the development of @DISEASE$, but the homogeneous 38AA genotype maybe one of the genetic markers for disease progression in Chinese IgA nephropathy.
[ "1" ]
857
857
Genetic polymorphism of XRCC1 R399Q is associated with response to platinum-based NAC in bulky @DISEASE$, and MDR analysis documented association between gene-gene interaction of @GENE$ R399Q and treatment response.
[ "1" ]
858
858
In conclusion, the results of the study in Korean @GENE$ 2 diabetic patients do not support the hypothesis that polymorphism at the 5' end of the aldose reductase gene contributes to the susceptibility to diabetic microvascular @DISEASE$.
[ "0" ]
859
859
These preliminary findings show for the first time that the @GENE$ His (213) allele is a possible risk factor for @DISEASE$ development.
[ "1" ]
860
860
We conclude that no significant association between I/D polymorphism and @DISEASE$ was demonstrable in either @GENE$ 1 or type 2 diabetes, despite considerable statistical power of the patient sample and adequate duration of diabetes for nephropathy to become manifest.
[ "0" ]
861
861
The expression of MIC genes on enterocytes under stressful conditions and their function as ligands of intraepithelial gammadelta and @GENE$ T cells, together with the data presented here suggest a potential role of MIC genes in the @DISEASE$ of CD.
[ "0" ]
862
862
The polymorphism of 8570G > A in @GENE$ may be associated with @DISEASE$ in the population of Han nationality from Hubei province of China.
[ "0" ]
863
863
Infant @GENE$ RR and PON2 CC genotypes were associated with preterm delivery in our study population, which suggests a possible role for human paraoxonase variability in the etiology of @DISEASE$.
[ "1" ]
864
864
Our data show that the exon 1 (+49) polymorphism of the @GENE$ gene is associated with @DISEASE$ in African Americans.
[ "1" ]
865
865
Despite the strikingly similar pathologies of @GENE$ syndrome and sarcoidosis, no mutations were found to be associated with @DISEASE$ in a group of patients, regardless of the presence of uveitis.
[ "1" ]
866
866
The present study demonstrates that the @GENE$ genotype of the Gly482Ser polymorphism in the PPARGC1 gene might be a risk factor for @DISEASE$ in the Slovene population (Caucasians) with type 2 diabetes (odds ratio 2.7, 95% confidence interval 1.0-6.8), whereas the Pro12Ala polymorphism of the PPARgamma gene failed to confer susceptibility to diabetic retinopathy.
[ "0" ]
867
867
Our results strongly suggest that the SNP of @GENE$ might be associated with susceptibility to @DISEASE$.
[ "0" ]
868
868
The association is found between the @DISEASE$ polymorphism and @GENE$, There is a significant correlation between the CC genotype of the APOA5 and the levels of plasma high density lipoprotein-cholosteal in the CHD group.
[ "0" ]
869
869
These results indicate that a genetic association exists between @GENE$ gene locus and severe @DISEASE$.
[ "0" ]
870
870
This is the first report that @GENE$, IL8, and PPARG genes are important in relation to inflammation-related risk of sporadic @DISEASE$.
[ "1" ]
871
871
these results may provide further support for an association between the @GENE$ gene (DTNBP1) and schizophrenia, but not between the @DISEASE$ and DAO, DAOA, NRG1 and RGS4 or with the interaction of these genes.
[ "0" ]
872
872
A positive correlation was found between LRP gene polymorphism and @DISEASE$, but not between @GENE$ gene polymorphism and AD in Chinese AD cases.
[ "1" ]
873
873
@GENE$ gene polymorphisms are not linked to @DISEASE$, suggesting that this gene does not have a role in the pathogenesis of optic neuropathy in this disease.
[ "0" ]
874
874
These results suggest that the rs1862214 polymorphism in PDCD5 is predictive for lung cancer risk and prognosis, and that @GENE$ may represent a novel tumor suppressor gene influencing @DISEASE$.
[ "1" ]
875
875
The impact of @GENE$ variants on risk of @DISEASE$ was mediated largely through the action of three common alleles, Arg151Cys, Arg160Trp, and Asp294His, that have previously been associated with red hair, fair skin, and skin sensitivity to ultraviolet light.
[ "1" ]
876
876
Our results suggest that the presence of the A-@GENE$ allele at the @DISEASE$ promoter region is associated with less aggressive forms of breast cancer and could be looked on as a favorable prognostic factor.
[ "0" ]
877
877
We provide evidence, for the first time, that @GENE$ promoter -514 C-->T polymorphism, by modulating LDL density, significantly affects the number of macrophages in the @DISEASE$ and possibly affects the occurrence of cerebrovascular events in patients with carotid artery stenosis.
[ "0" ]
878
878
Our data support a functional importance of the @GENE$ mutations for plasma concentrations and central @DISEASE$ actions of the opioid loperamide.
[ "0" ]
879
879
We conclude that the association of the FE65 intron @GENE$ polymorphism with @DISEASE$, if any, is smaller than previously reported.
[ "0" ]
880
880
None of the SNPs of KCNQ1 P448R, KCNQ1 R519H, KCNQ1 G643S, KCNE1 G38S and KCNE1 D85N was associated with atrial fibrillation phenotype, but @GENE$ E145D may relation to @DISEASE$.
[ "1" ]
881
881
Thus, there is a significant association between the PON1-192R allele and @DISEASE$; the @GENE$-192R allele may play an important role in the genesis of coronary spasm, probably by attenuating the suppression of oxidative stress.
[ "1" ]
882
882
The polymorphism in @GENE$ gene promoter (-173 G/C) does not appear to be genetic risk factors for @DISEASE$ in Northwest Spain.
[ "0" ]
883
883
In addition, these data suggest that @GENE$ repeat length may be partly responsible for the increased risk for early-onset @DISEASE$ in women who use OCs, although these findings need replication in other populations.
[ "1" ]
884
884
The results of our study suggest a role for the @GENE$ gene in modifying the clinical features of @DISEASE$.
[ "1" ]
885
885
We conclude that this study has failed to produce evidence in support of the notion that variations within these 24 candidate @GENE$ and asthma genes significantly influence the expression of the atopic @DISEASE$ phenotype or contribute to the susceptibility of atopic asthma.
[ "1" ]
886
886
These results suggested that the @GENE$ gene might be involved in the susceptibility to @DISEASE$ in the Chinese Han population and both +49 and CT60 of CTLA-4 gene might be the causal variants in RA disease.
[ "1" ]
887
887
Our data demonstrate that in B-@DISEASE$, plasma levels of @GENE$, IL-1Ra and IL-6 differ from normal, and mechanisms other than allelic imbalance of their genes account for the distinct cytokine profiles observed in this disease.
[ "0" ]
888
888
Our results suggest that the @GENE$ gene may play a minor role in the overall genetic predisposition to @DISEASE$ in this UK population.
[ "1" ]
889
889
These results suggested that among @GENE$ and related genes, IFNG and IRF1 genes confer genetic susceptibility to @DISEASE$ in Japanese children.
[ "1" ]
890
890
These results suggest that the @GENE$ gene is a target of genomic instability in MSI-positive @DISEASE$ and that the Chk1 framshift mutations might be involved in colorectal tumourigenesis through a defect in response to DNA damage in a subset of sporadic colorectal cancers and HNPCCs.
[ "1" ]
891
891
These results suggest no effect of the @GENE$ genotype on susceptibility to MS, but indicate an association of the APOE epsilon4 allele with a more severe course of the @DISEASE$.
[ "0" ]
892
892
This study identifies a novel genetic and clinical association between @GENE$ and @DISEASE$.
[ "0" ]
893
893
Our results suggest that the @GENE$ gene polymorphism may confer increased susceptibility to @DISEASE$.
[ "1" ]
894
894
Therefore, our results suggest that Glu298Asp @GENE$ polymorphism plays a role as a genetic susceptibility factor for @DISEASE$.
[ "1" ]
895
895
We conclude that the @GENE$ G(-174)C polymorphism is not associated with the risk of CAD or @DISEASE$ and does not contribute to cardiovascular risk stratification.
[ "1" ]
896
896
Together, our findings suggest that @GENE$ gene polymorphisms do not influence the susceptibility to @DISEASE$ or the clinical characteristics of MS in Japanese patients.
[ "1" ]
897
897
The A/T polymorphism of @GENE$ gene is associated with the risk factor for aneurysmal @DISEASE$.
[ "1" ]
898
898
The exon 3 @DISEASE$ in the @GENE$ predicts an improved response to pegvisomant therapy in acromegaly.
[ "0" ]
899
899
These results suggest the possibility that @GENE$ molecule play some part in formation of @DISEASE$, such as erythema nodosum in BD in Japanese.
[ "0" ]