bigbio/gad · Datasets at Hugging Face

id stringlengths 1 4	document_id stringlengths 1 4	text stringlengths 42 538	labels list
1600	1600	These studies support that MEF2A mutations are not a common cause of @DISEASE$ in white people and argue strongly against a role for the @GENE$ 21-bp deletion in autosomal dominant CAD.	[ "1" ]
1601	1601	The study indicated that 1784GC/CC genotypes of @GENE$ were significantly related with the elevated concentrations of serum TC and LDL-C in hypercholesterolemic subjects, and further work is necessary to confirm the role of 1784G > C polymorphism of SREBP-2 gene in the development of @DISEASE$.	[ "1" ]
1602	1602	Our data enrich the list of @GENE$ SNPs and could be useful to trigger further genetic studies about the involvement of DG in human @DISEASE$.	[ "0" ]
1603	1603	In conclusion, our results suggest that the @GENE$ gene or other genes in the region may increase the susceptibility to @DISEASE$ in men; however, the polymorphism in the 5' promoter region has a minor role if any in increasing prostate cancer susceptibility in our study sample.	[ "1" ]
1604	1604	The @GENE$-87T/C polymorphism is associated with higher fasting plasma glucose concentrations in both NGT and diabetic subjects, largely due to @DISEASE$ insulin sensitivity.	[ "0" ]
1605	1605	This study suggests that @GENE$ slow sulfation combined with higher intake of red meat may be associated with an elevated risk of @DISEASE$.	[ "0" ]
1606	1606	Our data suggested that the @GENE$ gene may contribute to the susceptibility of @DISEASE$ in the northern Han Chinese population, but further studies are needed to replicate these findings.	[ "1" ]
1607	1607	The haplotype of @GENE$ may serve as a novel genetic marker for the risk of @DISEASE$, coronary heart disease, and aortic dissection.	[ "0" ]
1608	1608	@GENE$ polymorphisms are a predisposing factor of melanoma in a southern European population with a relatively low incidence of the @DISEASE$.	[ "0" ]
1609	1609	The 67G allele of @GENE$ may be a contributing factor in the @DISEASE$ of SLE.	[ "0" ]
1610	1610	The results revealed a paucity of mutations in @GENE$/@DISEASE$, suggesting that in the Polish population this gene does not contribute significantly to either FMM or MM within the context of CFA.	[ "0" ]
1611	1611	Homozygous individuals for the -344C @GENE$ allele are at 17% lower risk of @DISEASE$ with respect to homozygous TT subjects.	[ "1" ]
1612	1612	It is unlikely that @GENE$ c.1-34T>C has a role in breast cancer etiology, overall or in combination with established non-genetic @DISEASE$ risk factors.	[ "1" ]
1613	1613	Homozygote @GENE$*28 allele carriers with higher serum bilirubin concentrations exhibit a strong association with lower risk of @DISEASE$.	[ "1" ]
1614	1614	These results suggest a role for the @GENE$ gene in susceptibility to diabetic nephropathy in @DISEASE$.	[ "1" ]
1615	1615	a polymorphism in the @GENE$ gene is shown for the first time to be associated with the clinical presentation of a malignant @DISEASE$ and more generally with the risk of distant tissue infiltration by tumor cells.	[ "0" ]
1616	1616	The small but significant effects of the 44-bp insertion/@DISEASE$ polymorphism for @GENE$ is consistent with being one of many genes that contributes to the multi-factorial nature of these psychiatric disorders.	[ "0" ]
1617	1617	These results @DISEASE$ to the evidence that certain HLA class @GENE$ alleles or allele combinations, or genes linked to them, make some women more susceptible to SCC.	[ "0" ]
1618	1618	Our data reveal that the @GENE$ 1188 (A-->C) gene polymorphism is not involved in defining the genetic basis of the susceptibility to and final outcome of @DISEASE$.	[ "1" ]
1619	1619	In conclusion, there was no association between the beta-fibrinogen -455 G/A, GP IIIa PlA1/A2, PAI-1 4G/5G, factor V Leiden 1691 G/A, TNFalpha -238 G/A, TNFalpha -308 G/A, IL-1alpha -889 C/T, the IL-1beta -511 C/T, @GENE$ 677 C/T and eNOS 4 b/a gene polymorphisms and the risk of @DISEASE$ after PTCA as well as recurrent restenosis after repeated PTCA.	[ "1" ]
1620	1620	The associated allele is previously shown to alter a transcription factor-binding site (@GENE$/AML1), and the results of this study suggest that this allele could act as an additional susceptibility allele to @DISEASE$.	[ "0" ]
1621	1621	Our results suggest that some allergic patients have @GENE$ @DISEASE$, and that L467P in the IFNGR1 gene is one of candidate susceptibility genes for allergic diseases.	[ "0" ]
1622	1622	The @GENE$ polymorphisms are not associated with disease susceptibility of @DISEASE$, but these genetic variations significantly influence phenotypes of sarcoidosis.	[ "1" ]
1623	1623	These results suggest no major modifying role for the Mn-@GENE$ gene polymorphism in patients with @DISEASE$.	[ "0" ]
1624	1624	These findings suggest that the CDT1 838G/A and GMNN 387C/A polymorphisms may not play a major role in the etiology of @DISEASE$, but @GENE$ variant may have a potential role only in genetically susceptible women.	[ "1" ]
1625	1625	Our results suggest that @GENE$ @DISEASE$ is not a major risk factor for morbidity or death in the adult Caucasian population.	[ "0" ]
1626	1626	The present study suggests that mutations in @GENE$ and CDH23 are the two major components of causes for @DISEASE$, while PCDH15, USH1C, and SANS are less frequent causes.	[ "0" ]
1627	1627	Our results @DISEASE$ to growing evidence that @GENE$ is associated with variation in weight, fat distribution and insulin resistance.	[ "0" ]
1628	1628	We conclude that the human @GENE$ gene is rather involved in the development of eosinophilia and changes in total IgE levels than contributing to the @DISEASE$ of asthma.	[ "0" ]
1629	1629	@GENE$ 936 C/C genotype or C allele is not related to the development of colorectal cancer, but they can reduce the risk of @DISEASE$ after surgery in colorectal cancer patients.	[ "0" ]
1630	1630	In this sample, MPO AA, associated with decreased production of @GENE$, was found to be a risk factor for @DISEASE$.	[ "1" ]
1631	1631	@GENE$ G972R was associated with the baseline characteristics of the patients with GDM, and might be related to insulin resistance that is seen in obese patients with @DISEASE$.	[ "1" ]
1632	1632	@GENE$-6 has minimal to no effect on the inter-individual variation of @DISEASE$ pressure levels, and is at best a 'minor gene' for blood pressure in the population as a whole.	[ "0" ]
1633	1633	A promoter polymorphism of @GENE$ (rs7528684) is associated with an increased risk of developing RA in Dutch Caucasians, suggesting that this association is relevant for @DISEASE$ in both Japanese and Caucasian populations.	[ "1" ]
1634	1634	Thus it seems advisable to carry out further examinations of the role of these polymorphisms in @DISEASE$ by means of @GENE$ method and the classical association method.	[ "0" ]
1635	1635	We compared our data with previous series and integrated the comprehension of molecular @GENE$ gene @DISEASE$ in heart development.	[ "0" ]
1636	1636	The @GENE$ epsilon 4 allele was associated with moderate to severe @DISEASE$ while no association between the IL-1 alpha gene polymorphism and AD was found.	[ "1" ]
1637	1637	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$.	[ "1" ]
1638	1638	We confirmed increased occurence of @DISEASE$ in patients with @GENE$, what stress importance of routine screening for OSA in patients with LADA.	[ "0" ]
1639	1639	We conclude that both @GENE$ and TNF-alpha can be candidate loci to be studied in the susceptibility to develop @DISEASE$.	[ "0" ]
1640	1640	our data suggests that the @GENE$ D allele is a modest risk factor for late-onset sporadic @DISEASE$ in Koreans, and the AD risk conferred by the A2M D allele increases in APOE epsilon4 negative subjects.	[ "1" ]
1641	1641	We therefore conclude that Tnfsf4 underlies Ath1 in mice and that polymorphisms in its human homolog @GENE$ increase the risk of @DISEASE$ in humans.	[ "1" ]
1642	1642	these results show the @GENE$ @DISEASE$ polymorphism is associated with prostate cancer risk.	[ "0" ]
1643	1643	We conclude that the @GENE$ Ia 807 TT (873 AA) genotype is associated with an increased risk of @DISEASE$ in the Italian population; conversely, the GP Ia 807 CC (873 GG) genotype seems to represent a protective factor.	[ "0" ]
1644	1644	The @DISEASE$ of @GENE$ ,89 site maybe one of important host susceptible factors of EC, and the risk would increase significantly in smokers.	[ "0" ]
1645	1645	These results suggest that the interaction between 5-HTTLPR and 5-@GENE$ polymorphisms may not contribute to susceptibility to @DISEASE$ as well as some clinical factors such as antipsychotic response, at least in the Korean population.	[ "1" ]
1646	1646	Our data suggest that @GENE$ plays some role in the development of @DISEASE$ in the Japanese population.	[ "0" ]
1647	1647	The observation that @GENE$ and CYP3A43 were associated with prostate cancer, are not in linkage equilibrium, and are both involved in testosterone metabolism, suggest that both CYP3A41B and CYP3A433 may influence the probability of having @DISEASE$ and disease severity.	[ "1" ]
1648	1648	Significant differences in the @GENE$ promoter polymorphism genotype frequency between northwest Spanish RA patients and controls suggest a potential role for this polymorphism in susceptibility to @DISEASE$.	[ "1" ]
1649	1649	Our results indicate that the @GENE$*S and apoE4 alleles have interactive effect on the development of the two most common forms of @DISEASE$ AD and VD, and further support the hypothesis that cardiovascular factors contribute to the development of AD.	[ "0" ]
1650	1650	Our results suggest that @DISEASE$ risk can be genetically modulated by @GENE$, which may repair DNA cross-link lesions produced by aromatic amines and other environmental chemicals.	[ "1" ]
1651	1651	No direct replication of previous OA association findings was obtained but the results suggest that the R324G SNP of the @GENE$ gene may have an effect in @DISEASE$ development in multiple joints, with a specific severe involvement of the hip in women.	[ "1" ]
1652	1652	We conclude that different haplotypes within the boundaries of the @GENE$ gene may be associated with @DISEASE$ in the Han Chinese.	[ "1" ]
1653	1653	Our data suggest that the @GENE$ 5' non-coding region polymorphism modulates NER capacity and is associated with decreased @DISEASE$ risk, especially in the presence of exposure to tobacco carcinogens.	[ "1" ]
1654	1654	We conclude that the @GENE$ gene polymorphism is not associated with @DISEASE$ in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.	[ "0" ]
1655	1655	As a conclusion, we could not find any significant association of @GENE$ variants with development of HCC among @DISEASE$ patients.	[ "0" ]
1656	1656	This study provides further evidence to support the role of @GENE$ in the @DISEASE$ of AAA, and indicates that the MMP9 C-1562T functional polymorphism may represent a genetic component contributing to susceptibility to this vascular disease.	[ "0" ]
1657	1657	Our data suggest that the @GENE$ gene mutation might be associated with early occurrence of @DISEASE$ and lower plasma levels of total and low density lipoprotein-cholesterol in the Chinese population.	[ "1" ]
1658	1658	Since the SH2D2A protein modulates T @GENE$ activation, this may be a mechanism for how short SH2D2A alleles confer susceptibility to develop @DISEASE$.	[ "0" ]
1659	1659	It was concluded that SP-B1580 T allele was probably associated with increased susceptibility to @DISEASE$ in Chinese Han population; The polymorphism of @GENE$-18A/C locus maybe varied with race.	[ "1" ]
1660	1660	In conclusion, the polymorphisms observed do not provide evidence to support a significant role for @GENE$ in @DISEASE$ susceptibility.	[ "1" ]
1661	1661	The results of present study suggest that the genetically determined low @GENE$ production may be the risk factor of @DISEASE$ development.	[ "0" ]
1662	1662	The present study demonstrates that polymorphisms of the @GENE$ -786T>C and 4a4b are associated with @DISEASE$ with adjustments for cardiovascular risk factors in the Koreans.	[ "1" ]
1663	1663	@GENE$ polymorphisms play no role in the genetic predisposition to @DISEASE$.	[ "1" ]
1664	1664	This study indicates a synergistic contribution of RAS genes (ACE I/D, @GENE$ T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature @DISEASE$.	[ "1" ]
1665	1665	No differences in frequencies of the @GENE$ deletion were found between controls and patients or between HLA-Cw6(+) and HLA-Cw6(-) controls or patients, suggesting that LILRA3 has no role in @DISEASE$.	[ "1" ]
1666	1666	These findings suggest that immunogenetic factors for susceptibility to gastric adenocarcinoma are present in the host, the @GENE$*04051 allele is a host genetic risk factor for @DISEASE$, and that this genetic risk is independent of H. pylori infection.	[ "1" ]
1667	1667	In this cohort of Hungarian children there was no association between - 28G, and - 403A alleles in the @GENE$ promoter, - 2518G polymorphism in the distal regulatory region of the MCP-1 and AEDS, or @DISEASE$.	[ "0" ]
1668	1668	These data demonstrate that the Arg(972) @GENE$ variant is associated with increased risk for @DISEASE$ failure to sulfonylurea, thus representing a potential example of pharmacogenetics in type 2 diabetes.	[ "0" ]
1669	1669	These data suggest that CYP1A1*4, @GENE$ and NAT2 variants are involved in the susceptibility to @DISEASE$ by modifying the impact of exogenous and/or endogenous exposures.	[ "1" ]
1670	1670	@GENE$ Arg399Gln polymorphism might contribute to the susceptibility to @DISEASE$.	[ "0" ]
1671	1671	The markedly greater @GENE$, proportionally larger than the greater BP, supports a role for RVR in the @DISEASE$ of EH.	[ "0" ]
1672	1672	We did not detect any linkage or association in these groups and conclude that if @GENE$ plays a role in typical migraine, it does not confer a major effect on the @DISEASE$.	[ "0" ]
1673	1673	Men who have the V allele of the @GENE$ gene have a twofold increase in the risk of @DISEASE$ development and an additional twofold increase in the risk of progression compared with men with the L/L genotype.	[ "1" ]
1674	1674	Our findings do not support the fact that the previously reported positive association between @GENE$ deletion polymorphism and @DISEASE$ modifies the disease risk in the studied population.	[ "1" ]
1675	1675	This report provides further support for the hypothesis that a single nucleotide polymorphism in the @GENE$ gene is a protective factor in lung cancer @DISEASE$.	[ "0" ]
1676	1676	These results indicate that @GENE$ gene variants do not contribute to PD @DISEASE$.	[ "0" ]
1677	1677	This study indicates that the 4G/5G gene polymorphism of PAI-1 is associated with @DISEASE$, that 4G/4G @GENE$ is probably an important hereditary risk factor, and that glucose has functional importance in regulating PAI-1 activity.	[ "0" ]
1678	1678	The @GENE$ exon 11 missense variant is not associated with @DISEASE$ in the CVCR.	[ "1" ]
1679	1679	We conclude that the @GENE$ insertion/@DISEASE$ variant does not show any significant association with the pathogenesis, fibrosis and progression of tropical calcific pancreatitis and the fibro-calculous pancreatic diabetes.	[ "0" ]
1680	1680	Our results suggest an important role for @GENE$ in major depression in women and also raise the possibility that previously proposed @DISEASE$-associated SNPs in the HTR3A/B region in Caucasians are in linkage disequilibrium with haplotype block 2 of HTR3B in the Japanese.	[ "0" ]
1681	1681	Val158Met polymorphism in @GENE$ gene could be a candidate for low penetrance breast cancer susceptibility in Shanghai population, especially among premenopausal women and early-onset @DISEASE$ patients.	[ "1" ]
1682	1682	We concluded that, the @GENE$ 49 A-G polymorphism is associated with @DISEASE$ in Chinese patients from Taiwan.	[ "1" ]
1683	1683	These results suggest that the @GENE$ gene region might be a susceptible locus to @DISEASE$ in Japanese.	[ "1" ]
1684	1684	We have therefore found no evidence of a causative role for @GENE$ in sebaceous gland @DISEASE$, and in the absence of any association between variation at the locus and disease group, the pathophysiologic role of the melanocortin 5 receptor in man requires further study.	[ "0" ]
1685	1685	Allele A in TNF-beta gene +252 site can significantly increase the relative risk of endometriosis in women in Guangdong, among which @GENE$ AA genotype might be one of the genetic susceptible factors for @DISEASE$.	[ "1" ]
1686	1686	This study suggests that @GENE$ C34T genotype is not a predictor of survival in @DISEASE$ patients, except possibly those with HxMI.	[ "0" ]
1687	1687	Our results demonstrate the association of the G972R variant of the @GENE$ gene with reduced @DISEASE$ in obese subjects, and indicate a possible interaction between the IRS-1 variant and obesity in worsening of insulin sensitivity.	[ "0" ]
1688	1688	These data suggest that the @GENE$ gene may confer susceptibility to the development of @DISEASE$ in the Chinese population.	[ "1" ]
1689	1689	Reactivity to microbial components is associated with severe @GENE$ characterized by small bowel involvement, frequent @DISEASE$, longer disease duration, and greater need for intestinal surgery.	[ "0" ]
1690	1690	These data suggest that the effect of @GENE$ genetic variation may be associated with negative symptoms in patients with @DISEASE$.	[ "1" ]
1691	1691	The difference in phenotypes between the two related heterozygotes, and the observation of @DISEASE$ in other family members without the mutation suggests that obesity results from a varying combination of environmental, behavioural and multiple genetic factors (other than @GENE$), even within the same family.	[ "1" ]
1692	1692	In this study, the first undertaken in Brazil into the association of @GENE$ deficiency and cystic fibrosis, we did not find an association between the deficiency and @DISEASE$ severity.	[ "1" ]
1693	1693	Contrary to previous reports the @GENE$ gene is not a major risk factor for @DISEASE$, nor is it a major determinant of disease progression.	[ "0" ]
1694	1694	The association found between TLR4 genotype and risk of @DISEASE$ suggests that @GENE$ genetic variants could potentially affect the susceptibility to MI and that TLR4-mediated innate immunity is implicated in the pathogenesis of MI.	[ "1" ]
1695	1695	@GENE$ gene polymorphisms cannot be applied as an effective genetic marker for @DISEASE$ susceptibility.	[ "0" ]
1696	1696	We conclude that common coding SNPs in the @GENE$ gene are unlikely to contribute significantly to increased IgE levels and variations outside the coding region may influence @DISEASE$ susceptibility.	[ "0" ]
1697	1697	The @GENE$ Ile-Val gene polymorphisms might be associated with the occurrence of @DISEASE$, while MspI gene polymorphisms and NAT2 slow acetylator genotype might not be associated with the occurrence of prostate cancer.	[ "1" ]
1698	1698	These results indicate that the T allele and TT genotype at @GENE$/-159 are risk factors for CAL in @DISEASE$, and that the development of CAL in KD may be related to the magnitude of CD14 toll-like receptor response.	[ "1" ]
1699	1699	Our results suggest that the @GENE$ receptor gene polymorphism does not confer increased susceptibility to @DISEASE$.	[ "1" ]

1600

These studies support that MEF2A mutations are not a common cause of @DISEASE$ in white people and argue strongly against a role for the @GENE$ 21-bp deletion in autosomal dominant CAD.

[ "1" ]

1601

The study indicated that 1784GC/CC genotypes of @GENE$ were significantly related with the elevated concentrations of serum TC and LDL-C in hypercholesterolemic subjects, and further work is necessary to confirm the role of 1784G > C polymorphism of SREBP-2 gene in the development of @DISEASE$.

[ "1" ]

1602

Our data enrich the list of @GENE$ SNPs and could be useful to trigger further genetic studies about the involvement of DG in human @DISEASE$.

[ "0" ]

1603

In conclusion, our results suggest that the @GENE$ gene or other genes in the region may increase the susceptibility to @DISEASE$ in men; however, the polymorphism in the 5' promoter region has a minor role if any in increasing prostate cancer susceptibility in our study sample.

[ "1" ]

1604

The @GENE$-87T/C polymorphism is associated with higher fasting plasma glucose concentrations in both NGT and diabetic subjects, largely due to @DISEASE$ insulin sensitivity.

[ "0" ]

1605

This study suggests that @GENE$ slow sulfation combined with higher intake of red meat may be associated with an elevated risk of @DISEASE$.

[ "0" ]

1606

Our data suggested that the @GENE$ gene may contribute to the susceptibility of @DISEASE$ in the northern Han Chinese population, but further studies are needed to replicate these findings.

[ "1" ]

1607

The haplotype of @GENE$ may serve as a novel genetic marker for the risk of @DISEASE$, coronary heart disease, and aortic dissection.

[ "0" ]

1608

@GENE$ polymorphisms are a predisposing factor of melanoma in a southern European population with a relatively low incidence of the @DISEASE$.

[ "0" ]

1609

The 67G allele of @GENE$ may be a contributing factor in the @DISEASE$ of SLE.

[ "0" ]

1610

The results revealed a paucity of mutations in @GENE$/@DISEASE$, suggesting that in the Polish population this gene does not contribute significantly to either FMM or MM within the context of CFA.

[ "0" ]

1611

Homozygous individuals for the -344C @GENE$ allele are at 17% lower risk of @DISEASE$ with respect to homozygous TT subjects.

[ "1" ]

1612

It is unlikely that @GENE$ c.1-34T>C has a role in breast cancer etiology, overall or in combination with established non-genetic @DISEASE$ risk factors.

[ "1" ]

1613

Homozygote @GENE$*28 allele carriers with higher serum bilirubin concentrations exhibit a strong association with lower risk of @DISEASE$.

[ "1" ]

1614

These results suggest a role for the @GENE$ gene in susceptibility to diabetic nephropathy in @DISEASE$.

[ "1" ]

1615

a polymorphism in the @GENE$ gene is shown for the first time to be associated with the clinical presentation of a malignant @DISEASE$ and more generally with the risk of distant tissue infiltration by tumor cells.

[ "0" ]

1616

The small but significant effects of the 44-bp insertion/@DISEASE$ polymorphism for @GENE$ is consistent with being one of many genes that contributes to the multi-factorial nature of these psychiatric disorders.

[ "0" ]

1617

These results @DISEASE$ to the evidence that certain HLA class @GENE$ alleles or allele combinations, or genes linked to them, make some women more susceptible to SCC.

[ "0" ]

1618

Our data reveal that the @GENE$ 1188 (A-->C) gene polymorphism is not involved in defining the genetic basis of the susceptibility to and final outcome of @DISEASE$.

[ "1" ]

1619

In conclusion, there was no association between the beta-fibrinogen -455 G/A, GP IIIa PlA1/A2, PAI-1 4G/5G, factor V Leiden 1691 G/A, TNFalpha -238 G/A, TNFalpha -308 G/A, IL-1alpha -889 C/T, the IL-1beta -511 C/T, @GENE$ 677 C/T and eNOS 4 b/a gene polymorphisms and the risk of @DISEASE$ after PTCA as well as recurrent restenosis after repeated PTCA.

[ "1" ]

1620

The associated allele is previously shown to alter a transcription factor-binding site (@GENE$/AML1), and the results of this study suggest that this allele could act as an additional susceptibility allele to @DISEASE$.

[ "0" ]

1621

Our results suggest that some allergic patients have @GENE$ @DISEASE$, and that L467P in the IFNGR1 gene is one of candidate susceptibility genes for allergic diseases.

[ "0" ]

1622

The @GENE$ polymorphisms are not associated with disease susceptibility of @DISEASE$, but these genetic variations significantly influence phenotypes of sarcoidosis.

[ "1" ]

1623

These results suggest no major modifying role for the Mn-@GENE$ gene polymorphism in patients with @DISEASE$.

[ "0" ]

1624

These findings suggest that the CDT1 838G/A and GMNN 387C/A polymorphisms may not play a major role in the etiology of @DISEASE$, but @GENE$ variant may have a potential role only in genetically susceptible women.

[ "1" ]

1625

Our results suggest that @GENE$ @DISEASE$ is not a major risk factor for morbidity or death in the adult Caucasian population.

[ "0" ]

1626

The present study suggests that mutations in @GENE$ and CDH23 are the two major components of causes for @DISEASE$, while PCDH15, USH1C, and SANS are less frequent causes.

[ "0" ]

1627

Our results @DISEASE$ to growing evidence that @GENE$ is associated with variation in weight, fat distribution and insulin resistance.

[ "0" ]

1628

We conclude that the human @GENE$ gene is rather involved in the development of eosinophilia and changes in total IgE levels than contributing to the @DISEASE$ of asthma.

[ "0" ]

1629

@GENE$ 936 C/C genotype or C allele is not related to the development of colorectal cancer, but they can reduce the risk of @DISEASE$ after surgery in colorectal cancer patients.

[ "0" ]

1630

In this sample, MPO AA, associated with decreased production of @GENE$, was found to be a risk factor for @DISEASE$.

[ "1" ]

1631

@GENE$ G972R was associated with the baseline characteristics of the patients with GDM, and might be related to insulin resistance that is seen in obese patients with @DISEASE$.

[ "1" ]

1632

@GENE$-6 has minimal to no effect on the inter-individual variation of @DISEASE$ pressure levels, and is at best a 'minor gene' for blood pressure in the population as a whole.

[ "0" ]

1633

A promoter polymorphism of @GENE$ (rs7528684) is associated with an increased risk of developing RA in Dutch Caucasians, suggesting that this association is relevant for @DISEASE$ in both Japanese and Caucasian populations.

[ "1" ]

1634

Thus it seems advisable to carry out further examinations of the role of these polymorphisms in @DISEASE$ by means of @GENE$ method and the classical association method.

[ "0" ]

1635

We compared our data with previous series and integrated the comprehension of molecular @GENE$ gene @DISEASE$ in heart development.

[ "0" ]

1636

The @GENE$ epsilon 4 allele was associated with moderate to severe @DISEASE$ while no association between the IL-1 alpha gene polymorphism and AD was found.

[ "1" ]

1637

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" ]

1638

We confirmed increased occurence of @DISEASE$ in patients with @GENE$, what stress importance of routine screening for OSA in patients with LADA.

[ "0" ]

1639

We conclude that both @GENE$ and TNF-alpha can be candidate loci to be studied in the susceptibility to develop @DISEASE$.

[ "0" ]

1640

our data suggests that the @GENE$ D allele is a modest risk factor for late-onset sporadic @DISEASE$ in Koreans, and the AD risk conferred by the A2M D allele increases in APOE epsilon4 negative subjects.

[ "1" ]

1641

We therefore conclude that Tnfsf4 underlies Ath1 in mice and that polymorphisms in its human homolog @GENE$ increase the risk of @DISEASE$ in humans.

[ "1" ]

1642

these results show the @GENE$ @DISEASE$ polymorphism is associated with prostate cancer risk.

[ "0" ]

1643

We conclude that the @GENE$ Ia 807 TT (873 AA) genotype is associated with an increased risk of @DISEASE$ in the Italian population; conversely, the GP Ia 807 CC (873 GG) genotype seems to represent a protective factor.

[ "0" ]

1644

The @DISEASE$ of @GENE$ ,89 site maybe one of important host susceptible factors of EC, and the risk would increase significantly in smokers.

[ "0" ]

1645

These results suggest that the interaction between 5-HTTLPR and 5-@GENE$ polymorphisms may not contribute to susceptibility to @DISEASE$ as well as some clinical factors such as antipsychotic response, at least in the Korean population.

[ "1" ]

1646

Our data suggest that @GENE$ plays some role in the development of @DISEASE$ in the Japanese population.

[ "0" ]

1647

The observation that @GENE$ and CYP3A43 were associated with prostate cancer, are not in linkage equilibrium, and are both involved in testosterone metabolism, suggest that both CYP3A4*1B and CYP3A43*3 may influence the probability of having @DISEASE$ and disease severity.

[ "1" ]

1648

Significant differences in the @GENE$ promoter polymorphism genotype frequency between northwest Spanish RA patients and controls suggest a potential role for this polymorphism in susceptibility to @DISEASE$.

[ "1" ]

1649

Our results indicate that the @GENE$*S and apoE4 alleles have interactive effect on the development of the two most common forms of @DISEASE$ AD and VD, and further support the hypothesis that cardiovascular factors contribute to the development of AD.

[ "0" ]

1650

Our results suggest that @DISEASE$ risk can be genetically modulated by @GENE$, which may repair DNA cross-link lesions produced by aromatic amines and other environmental chemicals.

[ "1" ]

1651

No direct replication of previous OA association findings was obtained but the results suggest that the R324G SNP of the @GENE$ gene may have an effect in @DISEASE$ development in multiple joints, with a specific severe involvement of the hip in women.

[ "1" ]

1652

We conclude that different haplotypes within the boundaries of the @GENE$ gene may be associated with @DISEASE$ in the Han Chinese.

[ "1" ]

1653

Our data suggest that the @GENE$ 5' non-coding region polymorphism modulates NER capacity and is associated with decreased @DISEASE$ risk, especially in the presence of exposure to tobacco carcinogens.

[ "1" ]

1654

We conclude that the @GENE$ gene polymorphism is not associated with @DISEASE$ in this Chinese population, but plasma ACE activity is genetically determined in the normotensive Chinese.

[ "0" ]

1655

As a conclusion, we could not find any significant association of @GENE$ variants with development of HCC among @DISEASE$ patients.

[ "0" ]

1656

This study provides further evidence to support the role of @GENE$ in the @DISEASE$ of AAA, and indicates that the MMP9 C-1562T functional polymorphism may represent a genetic component contributing to susceptibility to this vascular disease.

[ "0" ]

1657

Our data suggest that the @GENE$ gene mutation might be associated with early occurrence of @DISEASE$ and lower plasma levels of total and low density lipoprotein-cholesterol in the Chinese population.

[ "1" ]

1658

Since the SH2D2A protein modulates T @GENE$ activation, this may be a mechanism for how short SH2D2A alleles confer susceptibility to develop @DISEASE$.

[ "0" ]

1659

It was concluded that SP-B1580 T allele was probably associated with increased susceptibility to @DISEASE$ in Chinese Han population; The polymorphism of @GENE$-18A/C locus maybe varied with race.

[ "1" ]

1660

In conclusion, the polymorphisms observed do not provide evidence to support a significant role for @GENE$ in @DISEASE$ susceptibility.

[ "1" ]

1661

The results of present study suggest that the genetically determined low @GENE$ production may be the risk factor of @DISEASE$ development.

[ "0" ]

1662

The present study demonstrates that polymorphisms of the @GENE$ -786T>C and 4a4b are associated with @DISEASE$ with adjustments for cardiovascular risk factors in the Koreans.

[ "1" ]

1663

@GENE$ polymorphisms play no role in the genetic predisposition to @DISEASE$.

[ "1" ]

1664

This study indicates a synergistic contribution of RAS genes (ACE I/D, @GENE$ T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature @DISEASE$.

[ "1" ]

1665

No differences in frequencies of the @GENE$ deletion were found between controls and patients or between HLA-Cw6(+) and HLA-Cw6(-) controls or patients, suggesting that LILRA3 has no role in @DISEASE$.

[ "1" ]

1666

These findings suggest that immunogenetic factors for susceptibility to gastric adenocarcinoma are present in the host, the @GENE$*04051 allele is a host genetic risk factor for @DISEASE$, and that this genetic risk is independent of H. pylori infection.

[ "1" ]

1667

In this cohort of Hungarian children there was no association between - 28G, and - 403A alleles in the @GENE$ promoter, - 2518G polymorphism in the distal regulatory region of the MCP-1 and AEDS, or @DISEASE$.

[ "0" ]

1668

These data demonstrate that the Arg(972) @GENE$ variant is associated with increased risk for @DISEASE$ failure to sulfonylurea, thus representing a potential example of pharmacogenetics in type 2 diabetes.

[ "0" ]

1669

These data suggest that CYP1A1*4, @GENE$ and NAT2 variants are involved in the susceptibility to @DISEASE$ by modifying the impact of exogenous and/or endogenous exposures.

[ "1" ]

1670

@GENE$ Arg399Gln polymorphism might contribute to the susceptibility to @DISEASE$.

[ "0" ]

1671

The markedly greater @GENE$, proportionally larger than the greater BP, supports a role for RVR in the @DISEASE$ of EH.

[ "0" ]

1672

We did not detect any linkage or association in these groups and conclude that if @GENE$ plays a role in typical migraine, it does not confer a major effect on the @DISEASE$.

[ "0" ]

1673

Men who have the V allele of the @GENE$ gene have a twofold increase in the risk of @DISEASE$ development and an additional twofold increase in the risk of progression compared with men with the L/L genotype.

[ "1" ]

1674

Our findings do not support the fact that the previously reported positive association between @GENE$ deletion polymorphism and @DISEASE$ modifies the disease risk in the studied population.

[ "1" ]

1675

This report provides further support for the hypothesis that a single nucleotide polymorphism in the @GENE$ gene is a protective factor in lung cancer @DISEASE$.

[ "0" ]

1676

These results indicate that @GENE$ gene variants do not contribute to PD @DISEASE$.

[ "0" ]

1677

This study indicates that the 4G/5G gene polymorphism of PAI-1 is associated with @DISEASE$, that 4G/4G @GENE$ is probably an important hereditary risk factor, and that glucose has functional importance in regulating PAI-1 activity.

[ "0" ]

1678

The @GENE$ exon 11 missense variant is not associated with @DISEASE$ in the CVCR.

[ "1" ]

1679

We conclude that the @GENE$ insertion/@DISEASE$ variant does not show any significant association with the pathogenesis, fibrosis and progression of tropical calcific pancreatitis and the fibro-calculous pancreatic diabetes.

[ "0" ]

1680

Our results suggest an important role for @GENE$ in major depression in women and also raise the possibility that previously proposed @DISEASE$-associated SNPs in the HTR3A/B region in Caucasians are in linkage disequilibrium with haplotype block 2 of HTR3B in the Japanese.

[ "0" ]

1681

Val158Met polymorphism in @GENE$ gene could be a candidate for low penetrance breast cancer susceptibility in Shanghai population, especially among premenopausal women and early-onset @DISEASE$ patients.

[ "1" ]

1682

We concluded that, the @GENE$ 49 A-G polymorphism is associated with @DISEASE$ in Chinese patients from Taiwan.

[ "1" ]

1683

These results suggest that the @GENE$ gene region might be a susceptible locus to @DISEASE$ in Japanese.

[ "1" ]

1684

We have therefore found no evidence of a causative role for @GENE$ in sebaceous gland @DISEASE$, and in the absence of any association between variation at the locus and disease group, the pathophysiologic role of the melanocortin 5 receptor in man requires further study.

[ "0" ]

1685

Allele A in TNF-beta gene +252 site can significantly increase the relative risk of endometriosis in women in Guangdong, among which @GENE$ AA genotype might be one of the genetic susceptible factors for @DISEASE$.

[ "1" ]

1686

This study suggests that @GENE$ C34T genotype is not a predictor of survival in @DISEASE$ patients, except possibly those with HxMI.

[ "0" ]

1687

Our results demonstrate the association of the G972R variant of the @GENE$ gene with reduced @DISEASE$ in obese subjects, and indicate a possible interaction between the IRS-1 variant and obesity in worsening of insulin sensitivity.

[ "0" ]

1688

These data suggest that the @GENE$ gene may confer susceptibility to the development of @DISEASE$ in the Chinese population.

[ "1" ]

1689

Reactivity to microbial components is associated with severe @GENE$ characterized by small bowel involvement, frequent @DISEASE$, longer disease duration, and greater need for intestinal surgery.

[ "0" ]

1690

These data suggest that the effect of @GENE$ genetic variation may be associated with negative symptoms in patients with @DISEASE$.

[ "1" ]

1691

The difference in phenotypes between the two related heterozygotes, and the observation of @DISEASE$ in other family members without the mutation suggests that obesity results from a varying combination of environmental, behavioural and multiple genetic factors (other than @GENE$), even within the same family.

[ "1" ]

1692

In this study, the first undertaken in Brazil into the association of @GENE$ deficiency and cystic fibrosis, we did not find an association between the deficiency and @DISEASE$ severity.

[ "1" ]

1693

Contrary to previous reports the @GENE$ gene is not a major risk factor for @DISEASE$, nor is it a major determinant of disease progression.

[ "0" ]

1694

The association found between TLR4 genotype and risk of @DISEASE$ suggests that @GENE$ genetic variants could potentially affect the susceptibility to MI and that TLR4-mediated innate immunity is implicated in the pathogenesis of MI.

[ "1" ]

1695

@GENE$ gene polymorphisms cannot be applied as an effective genetic marker for @DISEASE$ susceptibility.

[ "0" ]

1696

We conclude that common coding SNPs in the @GENE$ gene are unlikely to contribute significantly to increased IgE levels and variations outside the coding region may influence @DISEASE$ susceptibility.

[ "0" ]

1697

The @GENE$ Ile-Val gene polymorphisms might be associated with the occurrence of @DISEASE$, while MspI gene polymorphisms and NAT2 slow acetylator genotype might not be associated with the occurrence of prostate cancer.

[ "1" ]

1698

These results indicate that the T allele and TT genotype at @GENE$/-159 are risk factors for CAL in @DISEASE$, and that the development of CAL in KD may be related to the magnitude of CD14 toll-like receptor response.

[ "1" ]

1699

Our results suggest that the @GENE$ receptor gene polymorphism does not confer increased susceptibility to @DISEASE$.

[ "1" ]