bigbio/gad · Datasets at Hugging Face

id stringlengths 1 4	document_id stringlengths 1 4	text stringlengths 42 538	labels list
600	600	We found no significant association of @DISEASE$ with the trinucleotide repeat polymorphism of the @GENE$ or VLDLR genes, suggesting that these polymorphisms do not have a major role in the pathogenesis of the disease.	[ "1" ]
601	601	We conclude that @GENE$ is not a major or independent determinant in the occurrence of @DISEASE$ in the Chinese Han population.	[ "1" ]
602	602	These results strongly argue against a major role of @GENE$ polymorphisms in the @DISEASE$ of type 2 diabetes.	[ "0" ]
603	603	These data suggest that genetic polymorphisms in @GENE$, UGT1A6 and in UGT1A8 do not predispose to the development of @DISEASE$ in Caucasians.	[ "0" ]
604	604	The findings are consistent with evidence that, in addition to the widely described Y402H variant, there is at least one and, most probably, several other mutations in the @GENE$ gene which determine @DISEASE$ manifestation in AMD.	[ "0" ]
605	605	We therefore conclude that although @GENE$ gene does not seem to be primarily associated with CD, it might be a component of the high risk haplotype, playing a role as an additional predisposing gene for the @DISEASE$.	[ "0" ]
606	606	These findings suggest that @GENE$, MMP-3, and MMP-9 gene polymorphisms account for some of the variability in the @DISEASE$ of HCV-related chronic liver diseases.	[ "0" ]
607	607	When the dose of lansoprazole is decreased, the @GENE$ genotype of CYP2C19 appears to be a risk factor for symptomatic @DISEASE$ of GERD.	[ "0" ]
608	608	Variants in the regulatory region shared by PARK2 and @GENE$ therefore act as common risk factors for @DISEASE$.	[ "1" ]
609	609	it is unlikely that common variants in @GENE$, MLH3, PMS1, MSH2, MSH3 and MSH6 contribute significantly to @DISEASE$ susceptibility.	[ "1" ]
610	610	In conclusion, the single @GENE$ pair polymorphism of CD14 promoter gene is associated with CD14 expression and Chlamydia-stimulated TNFalpha production, and may thus play some role in the chlamydia-induced @DISEASE$.	[ "0" ]
611	611	Our results demonstrate for the first time that the @GENE$ polymorphism is a genetic susceptibility factor for the occurrence and @DISEASE$ of ESCC.	[ "0" ]
612	612	The C242T @GENE$ polymorphism is associated with @DISEASE$.	[ "0" ]
613	613	our data provide further evidence that specific genes may be involved in different @DISEASE$ subtypes and suggest that the @GENE$ gene deserves further study as a general susceptibility gene for schizophrenia.	[ "1" ]
614	614	These observations of higher frequency of the 5-HTTLPR S allele in subjects with past/present @DISEASE$ fit with previous findings and point to the important role of @GENE$ in depression.	[ "1" ]
615	615	We did not find significant evidence to support an association of MMP-3 allele 5A or @GENE$ allele 2G with @DISEASE$ in Norwegian and Swedish populations.	[ "1" ]
616	616	These data represent an important negative @DISEASE$ and suggest that, while @GENE$ is implicated in rare Mendelian susceptibility to mycobacterial disease, the common variants studied here do not have a major influence on susceptibility to pulmonary TB in The Gambian population.	[ "0" ]
617	617	The 77C-->G transition in exon 4 of the @GENE$ gene may contribute to @DISEASE$ susceptibility only in very few families, if at all, but it is not relevant for the majority of MS cases, including virtually all German patients.	[ "1" ]
618	618	In conclusion, our data suggest that the @GENE$*D allele could lead to genetic susceptibility to @DISEASE$ in Poles.	[ "0" ]
619	619	We conclude, that the Gly482Ser variant in @GENE$ is not associated with @DISEASE$-related traits or skeletal muscle fiber type composition in a non-diabetic German and Dutch population.	[ "0" ]
620	620	The effect of the @GENE$*1F @DISEASE$ on CYP1A2 activity in smoking pregnant women could not be confirmed.	[ "0" ]
621	621	We found no evidence that @GENE$ and PTEN germline mutations are associated with @DISEASE$ risk in Jews.	[ "1" ]
622	622	Our data do not suggest an excess of @GENE$ rare alleles among adult @DISEASE$ cases.	[ "1" ]
623	623	it is unlikely that variation in @GENE$ plays a major role in the pathogenesis of @DISEASE$ in the examined cohorts.	[ "1" ]
624	624	These findings indicated that the polymorphism of CD14 but not TLR4 Asp299Gly mutation was associated with Chinese patients with colorectal cancer, and the @GENE$ gene may contribute to the predisposition to @DISEASE$.	[ "1" ]
625	625	The co-existence of the 4G/5G polymorphism of the @GENE$ activator inhibitor type 1 gene and the I/D polymorphism of the angiotensin-converting enzyme gene increases the risk for early onset of @DISEASE$ in this population.	[ "0" ]
626	626	These results suggest that sequence variants in this gene are associated with @DISEASE$ risk, presumably through defective DNA repair function of @GENE$.	[ "1" ]
627	627	These findings indicate that CCR5 59029 is a host genetic factor that is associated with responses to @GENE$ therapy among Japanese patients with @DISEASE$.	[ "0" ]
628	628	Although a possible interaction between CYP17 gene C/T polymorphism and @GENE$ has been reported in the literature, we did not find any evidence for this the difference among clinical staging, pathological grading, or responsiveness to hormonal therapy in @DISEASE$.	[ "0" ]
629	629	@GENE$ mutations, originally linked to @DISEASE$, may act as a genetic susceptibility factor for other inflammatory disorders such as vascular BD.	[ "0" ]
630	630	The association between the @GENE$ G allele and early @DISEASE$ is largely explained by individuals with RA who have coexisting autoimmune endocrinopathies.	[ "1" ]
631	631	Mutational analysis of the @GENE$ gene in a series of Italian patients revealed one novel mutation and confirmed an important role played by this gene in a significant proportion of patients affected by @DISEASE$, when it is inherited as an autosomal dominant trait with variable expressivity and incomplete penetrance.	[ "1" ]
632	632	The presence of the C allele in the -174 position in the gene coding for @GENE$ could play a role in the pathology of @DISEASE$ following IAI in the mother and probably is connected with decreased of immunological reaction.	[ "1" ]
633	633	Our results suggest an important role for HTR3B in @DISEASE$ in women and also raise the possibility that previously proposed disease-associated SNPs in the @GENE$/B region in Caucasians are in linkage disequilibrium with haplotype block 2 of HTR3B in the Japanese.	[ "1" ]
634	634	In @DISEASE$, @GENE$ 4G/5G gene polymorphism may have a significant role in the occurrence of fatal and non-fatal MI.	[ "0" ]
635	635	These results suggest that the UGT2B15 enzyme may have a role in the metabolism of dihydrotestosterone in prostate tissue and @GENE$ Asp85Tyr polymorphism is associated with @DISEASE$ risk.	[ "1" ]
636	636	@GENE$ G972R was associated with the baseline characteristics of the patients with @DISEASE$, and might be related to insulin resistance that is seen in obese patients with GDM.	[ "1" ]
637	637	The @GENE$ Asp allele may be a genetic risk factor for @DISEASE$, and might influence the course of Alzheimer disease, even though effects vary in different studies.	[ "0" ]
638	638	Our results strongly suggest that polymorphism in the @GENE$ promoter region might be associated with susceptibility to @DISEASE$.	[ "1" ]
639	639	This is the first report that demonstrates that the rare polymorphisms at codons 119 and 432 of @GENE$ gene have higher risk for endometrial cancer, and positive correlations with ERalpha and ERbeta expressions in @DISEASE$.	[ "1" ]
640	640	The study results suggest that the three @GENE$ gene polymorphisms are unlikely to be major genetic susceptibility factors for @DISEASE$ in the northern Han Chinese population.	[ "0" ]
641	641	We found evidence for association between @GENE$ and COGA @DISEASE$, history of blackouts, age at first drunkenness, and level of response to alcohol.	[ "1" ]
642	642	The lack of association between @GENE$ genotypes and IgE as well as atopic outcomes in this large German study population seems to indicate that CD14 genotypes may not directly be involved in the development of @DISEASE$ during childhood.	[ "0" ]
643	643	These results support the hypothesis that the Sl2 allele and, possibly, the @GENE$ allele evolved in the context of @DISEASE$ transmission and that in certain combinations probably confer a survival advantage on these populations.	[ "0" ]
644	644	Our results indicate that genetic polymorphisms affecting knee @DISEASE$ vary between populations (Japanese versus Caucasian) and sexes and indicate a role for @GENE$, COMP, FRZB, and COL2A1 in Caucasians.	[ "1" ]
645	645	For a similar level of exposure to established carcinogens, individuals with the @GENE$ A-allele genotypes appear to have a reduced risk of @DISEASE$.	[ "1" ]
646	646	Our findings do not indicate a role for the @GENE$ T-C polymorphism in @DISEASE$, but a role in male carriers of a BRCA2 mutation could not be excluded because of the small sample size.	[ "0" ]
647	647	The @GENE$ gene polymorphism, especially an increase in the frequency of the L allele, was found to be associated with @DISEASE$.	[ "0" ]
648	648	These data suggest that @GENE$ 82S upregulates the @DISEASE$ upon engagement of S100/calgranulins, and, thereby, may contribute to enhanced proinflammatory mechanisms in immune/inflammatory diseases.	[ "0" ]
649	649	The Bst U I polymorphism of the @GENE$ gene is a suitable genetic marker of @DISEASE$ but cannot be used in the prediction of the outcome of patients who have received hormonal therapy.	[ "1" ]
650	650	The Pro/Pro genotype of @GENE$ codon 72 appears to be an independent prognostic marker in @DISEASE$ patients.	[ "1" ]
651	651	We conclude that a different distribution of BMI could influence the results of analyses of @GENE$ gene polymorphisms in @DISEASE$-control studies.	[ "0" ]
652	652	The strong @DISEASE$ predisposition conferred by the @GENE$ and CFH SNPs may result from biological epistasis, because ERCC6 functions in universal transcription as a component of RNA pol I transcription complex.	[ "1" ]
653	653	@GENE$ 49 AA is protective from diabetes mellitus, whereas, CTLA-4 49 G allele (both as homozygotes and as heterozygotes ) confers an increased risk of @DISEASE$.	[ "1" ]
654	654	We conclude that APOE genotype influences the cellular distribution of increased reducible @GENE$ adduct accumulation in @DISEASE$.	[ "0" ]
655	655	Our results suggest MMP-2 and @GENE$ genotypes play a crucial role in gastric cancer invasion, but not with development of @DISEASE$.	[ "1" ]
656	656	The haplotype formed by 5 SNPs in the @GENE$ gene may be associated with type 2 diabetes in Han population of China, which is confirmed from statistics to be a susceptibility gene for the @DISEASE$.	[ "0" ]
657	657	A common variant of @GENE$, previously associated with a lower AHSG protein level, is thus more common among lean than obese and @DISEASE$ men, supporting the results from Ahsg knock-out mice, namely, that AHSG modulates body mass.	[ "0" ]
658	658	In conclusion, this is the first study to show that the @GENE$ T2854G variants are associated with elevated postprandial @DISEASE$ concentrations in the study population of Korean men.	[ "0" ]
659	659	The present findings indicated that certain alleles or genotypes of the @GENE$ gene may confer a susceptibility of @DISEASE$, especially of the hebephrenic type.	[ "1" ]
660	660	These data suggest a role for the @GENE$ I interferon pathway in resistance to @DISEASE$.	[ "0" ]
661	661	The current findings indicate that the IL-17F H161R variant influences the risk of asthma and is a natural IL-17F antagonist, suggesting a potential role for @GENE$ in the etiology of @DISEASE$.	[ "1" ]
662	662	Our results suggest a role of @GENE$ in the @DISEASE$ of CAL and might explain the excess of males affected with KD.	[ "0" ]
663	663	C311S polymorphism of @GENE$ has no significant correlation with @DISEASE$ in Han people of Chinese Hunan area and allele C/S is not an independent risk factor for stroke,neither is G148A.	[ "1" ]
664	664	The current study does not support the notion that the polymorphism in the @GENE$ gene constitutes a risk factor for either late-onset or early-onset @DISEASE$, which means that other genetic factors play a role in the development of AD in the Italian population.	[ "1" ]
665	665	The current results show that variation at the rs6295 polymorphism of the @GENE$ gene is not associated with @DISEASE$ generally.	[ "0" ]
666	666	Among postmenopausal Caucasian women, common variants of the @GENE$ gene are not associated with risk of @DISEASE$.	[ "1" ]
667	667	In our study, no correlation was detected between the polymorphism of @GENE$ gene and @DISEASE$.	[ "0" ]
668	668	The variant 180A>G (A60A) in @GENE$ is a risk factor for @DISEASE$, and a dynamic equilibrium of genes in HOX paralog 13 is involved in the pathogenesis of cryptorchidism.	[ "0" ]
669	669	The wild-@GENE$ allele of the TNF-alpha promoter polymorphism may be associated with mechanisms of @DISEASE$ sensitivity to inhaled SO2.	[ "0" ]
670	670	These data provide evidences for the contributions of exon2 and exon13 polymorphisms of @GENE$ to susceptibility to @DISEASE$ in Chinese Han population surrounding province.	[ "0" ]
671	671	PADI4 is significantly overexpressed in the blood of @DISEASE$ patients but genetic variation within @GENE$ is not a major risk factor for RA in Caucasians.	[ "1" ]
672	672	Together, our findings suggest that IL-1beta or @GENE$ gene polymorphisms may not be relevant in the susceptibility to @DISEASE$ or the clinical characteristics of Japanese patients with MS.	[ "0" ]
673	673	Genetic variations in @GENE$ or ADIPOR2 are unlikely to lead to a common genetic predisposition to insulin resistance or @DISEASE$ in the Japanese population.	[ "1" ]
674	674	demonstrated that neither single marker nor haplotype analysis revealed an association between variants at the @GENE$ locus and @DISEASE$, suggesting that it is unlikely that the GRIP1 polymorphisms investigated play a substantial role in conferring susceptibility to schizophrenia.	[ "1" ]
675	675	Thus, the @GENE$-1alpha gene locus influences carbohydrate metabolism and contributes to @DISEASE$ in the population studied.	[ "0" ]
676	676	The possible modifying effect on MBC risk in subjects carrying @GENE$/2 germ-line mutations of an occupation characterised by exposure to chemicals such as polycyclic aromatic hydrocarbons (PAH) that are capable of inducing @DISEASE$, may provide clues to the role of environmental exposures in modifying BC risk in mutation carriers in both genders.	[ "0" ]
677	677	Our data did not support the hypothesis that @GENE$ and/or MMP-3 gene promoter polymorphisms influenced the susceptibility to @DISEASE$ in Japanese patients, indicating MMP-1 and MMP-3 expressions were regulated by complex processes such as cytokine network in periodontal disease rather than gene polymorphisms.	[ "1" ]
678	678	These results suggest that a genetic polymorphism in the 5' flanking region of the @GENE$ gene would be associated with @DISEASE$ in lupus through modulating MCP-1 expression.	[ "0" ]
679	679	The @GENE$-232C > G polymorphism is not a major contributor to the pathogenesis of @DISEASE$ in the Danish population.	[ "1" ]
680	680	This report identifies a genetic association in humans between @DISEASE$ and @GENE$ class II and III genes.	[ "0" ]
681	681	The @GENE$ polymorphisms studied do not contribute to @DISEASE$ susceptibility in Japanese or Dutch sarcoidosis patients.	[ "0" ]
682	682	The @GENE$ C2 variant did not confer a risk for @DISEASE$ in Koreans.	[ "1" ]
683	683	If confirmed by others, our results indicate that more intensive @DISEASE$ prophylaxis is needed for patients with at least one @GENE$ G allele, possibly directed toward blunting early host cell production of IL-2.	[ "1" ]
684	684	In conclusion, alterations in the @GENE$ gene are unlikely to contribute importantly to the pathogenesis of @DISEASE$ or lipoatrophic diabetes mellitus in Japan.	[ "1" ]
685	685	@GENE$ germline genetic variation affects @DISEASE$ susceptibility, and possibly survival, in PMF, regardless of VF mutational status.	[ "0" ]
686	686	We conclude that genetic variants at the @GENE$ locus occur commonly in subjects with this @DISEASE$ (four out of 18 subjects with probably functional mutants) and may affect the individual's response to obesity and diabetes mellitus for the development of lipaemia.	[ "0" ]
687	687	Our results suggest that the G908R mutation of the CARD15/NOD2 gene, as well as the T allele and TT genotype of the @GENE$ promoter are associated with increased susceptibility for developing @DISEASE$.	[ "1" ]
688	688	The results suggest that the investigated BDNF polymorphisms are neither robust genetic risk factors nor determinants of @GENE$ protein levels in @DISEASE$.	[ "1" ]
689	689	the Gilbert @GENE$ allele increases the risk of @DISEASE$ formation in CF.	[ "1" ]
690	690	The @GENE$ genotype is an important genetic marker predicting an individual's predisposition to @DISEASE$.	[ "1" ]
691	691	Replication of the original @GENE$ findings in these 4 additional @DISEASE$ populations suggests that this gene (and perhaps others that interact with it) is important in the development and pathogenesis of asthma.	[ "1" ]
692	692	This study provides further evidence that sequence variation in @GENE$ is associated with an increased risk of breast cancer, and implies that @DISEASE$ in association with CHEK2 mutations does not involve loss of the wild type allele.	[ "0" ]
693	693	This new marker may provide a valuable tool to assess the risk for @GENE$-associated @DISEASE$, but it does not appear to be associated with asthma and/or atopy.	[ "0" ]
694	694	In the present study, we found that short polymorphic genotypes of [TTTA]n repeats of the @GENE$ gene were associated with @DISEASE$ risk.	[ "0" ]
695	695	a genetic polymorphism links MPO expression to Alzheimer's risk, in that a higher expressing SpSp MPO genotype was associated with increased incidence of @DISEASE$ in females, and decreased incidence in males (@GENE$.006)	[ "0" ]
696	696	Our findings provide further support that @GENE$ is a modifying gene that plays a role in determining interindividual variability in the proclivity for outward and self-directed @DISEASE$ found in some schizophrenic patients.	[ "0" ]
697	697	In contrast to other PPIs, esomeprazole-induced healing of @DISEASE$ is unrelated to the CYP2C19 genotype, which can be explained by the metabolic shift toward the @GENE$-mediated pathway.	[ "0" ]
698	698	The present findings show that the preferential Th2-@GENE$ response to @DISEASE$ was associated with a poorer prognosis and suggest that polymorphisms of the IL-4Ralpha gene may serve as useful genetic markers for assessing the risk of the development and progression of RCC.	[ "0" ]
699	699	In this study population, the authors were unable to confirm that the polymorphism of @GENE$-adrenergic receptor gene is a crucial factor of the susceptibility to @DISEASE$ and a major genetic determinant of different clinical status.	[ "0" ]

600

We found no significant association of @DISEASE$ with the trinucleotide repeat polymorphism of the @GENE$ or VLDLR genes, suggesting that these polymorphisms do not have a major role in the pathogenesis of the disease.

[ "1" ]

601

We conclude that @GENE$ is not a major or independent determinant in the occurrence of @DISEASE$ in the Chinese Han population.

[ "1" ]

602

These results strongly argue against a major role of @GENE$ polymorphisms in the @DISEASE$ of type 2 diabetes.

[ "0" ]

603

These data suggest that genetic polymorphisms in @GENE$, UGT1A6 and in UGT1A8 do not predispose to the development of @DISEASE$ in Caucasians.

[ "0" ]

604

The findings are consistent with evidence that, in addition to the widely described Y402H variant, there is at least one and, most probably, several other mutations in the @GENE$ gene which determine @DISEASE$ manifestation in AMD.

[ "0" ]

605

We therefore conclude that although @GENE$ gene does not seem to be primarily associated with CD, it might be a component of the high risk haplotype, playing a role as an additional predisposing gene for the @DISEASE$.

[ "0" ]

606

These findings suggest that @GENE$, MMP-3, and MMP-9 gene polymorphisms account for some of the variability in the @DISEASE$ of HCV-related chronic liver diseases.

[ "0" ]

607

When the dose of lansoprazole is decreased, the @GENE$ genotype of CYP2C19 appears to be a risk factor for symptomatic @DISEASE$ of GERD.

[ "0" ]

608

Variants in the regulatory region shared by PARK2 and @GENE$ therefore act as common risk factors for @DISEASE$.

[ "1" ]

609

it is unlikely that common variants in @GENE$, MLH3, PMS1, MSH2, MSH3 and MSH6 contribute significantly to @DISEASE$ susceptibility.

[ "1" ]

610

In conclusion, the single @GENE$ pair polymorphism of CD14 promoter gene is associated with CD14 expression and Chlamydia-stimulated TNFalpha production, and may thus play some role in the chlamydia-induced @DISEASE$.

[ "0" ]

611

Our results demonstrate for the first time that the @GENE$ polymorphism is a genetic susceptibility factor for the occurrence and @DISEASE$ of ESCC.

[ "0" ]

612

The C242T @GENE$ polymorphism is associated with @DISEASE$.

[ "0" ]

613

our data provide further evidence that specific genes may be involved in different @DISEASE$ subtypes and suggest that the @GENE$ gene deserves further study as a general susceptibility gene for schizophrenia.

[ "1" ]

614

These observations of higher frequency of the 5-HTTLPR S allele in subjects with past/present @DISEASE$ fit with previous findings and point to the important role of @GENE$ in depression.

[ "1" ]

615

We did not find significant evidence to support an association of MMP-3 allele 5A or @GENE$ allele 2G with @DISEASE$ in Norwegian and Swedish populations.

[ "1" ]

616

These data represent an important negative @DISEASE$ and suggest that, while @GENE$ is implicated in rare Mendelian susceptibility to mycobacterial disease, the common variants studied here do not have a major influence on susceptibility to pulmonary TB in The Gambian population.

[ "0" ]

617

The 77C-->G transition in exon 4 of the @GENE$ gene may contribute to @DISEASE$ susceptibility only in very few families, if at all, but it is not relevant for the majority of MS cases, including virtually all German patients.

[ "1" ]

618

In conclusion, our data suggest that the @GENE$*D allele could lead to genetic susceptibility to @DISEASE$ in Poles.

[ "0" ]

619

We conclude, that the Gly482Ser variant in @GENE$ is not associated with @DISEASE$-related traits or skeletal muscle fiber type composition in a non-diabetic German and Dutch population.

[ "0" ]

620

The effect of the @GENE$*1F @DISEASE$ on CYP1A2 activity in smoking pregnant women could not be confirmed.

[ "0" ]

621

We found no evidence that @GENE$ and PTEN germline mutations are associated with @DISEASE$ risk in Jews.

[ "1" ]

622

Our data do not suggest an excess of @GENE$ rare alleles among adult @DISEASE$ cases.

[ "1" ]

623

it is unlikely that variation in @GENE$ plays a major role in the pathogenesis of @DISEASE$ in the examined cohorts.

[ "1" ]

624

These findings indicated that the polymorphism of CD14 but not TLR4 Asp299Gly mutation was associated with Chinese patients with colorectal cancer, and the @GENE$ gene may contribute to the predisposition to @DISEASE$.

[ "1" ]

625

The co-existence of the 4G/5G polymorphism of the @GENE$ activator inhibitor type 1 gene and the I/D polymorphism of the angiotensin-converting enzyme gene increases the risk for early onset of @DISEASE$ in this population.

[ "0" ]

626

These results suggest that sequence variants in this gene are associated with @DISEASE$ risk, presumably through defective DNA repair function of @GENE$.

[ "1" ]

627

These findings indicate that CCR5 59029 is a host genetic factor that is associated with responses to @GENE$ therapy among Japanese patients with @DISEASE$.

[ "0" ]

628

Although a possible interaction between CYP17 gene C/T polymorphism and @GENE$ has been reported in the literature, we did not find any evidence for this the difference among clinical staging, pathological grading, or responsiveness to hormonal therapy in @DISEASE$.

[ "0" ]

629

@GENE$ mutations, originally linked to @DISEASE$, may act as a genetic susceptibility factor for other inflammatory disorders such as vascular BD.

[ "0" ]

630

The association between the @GENE$ G allele and early @DISEASE$ is largely explained by individuals with RA who have coexisting autoimmune endocrinopathies.

[ "1" ]

631

Mutational analysis of the @GENE$ gene in a series of Italian patients revealed one novel mutation and confirmed an important role played by this gene in a significant proportion of patients affected by @DISEASE$, when it is inherited as an autosomal dominant trait with variable expressivity and incomplete penetrance.

[ "1" ]

632

The presence of the C allele in the -174 position in the gene coding for @GENE$ could play a role in the pathology of @DISEASE$ following IAI in the mother and probably is connected with decreased of immunological reaction.

[ "1" ]

633

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

[ "1" ]

634

In @DISEASE$, @GENE$ 4G/5G gene polymorphism may have a significant role in the occurrence of fatal and non-fatal MI.

[ "0" ]

635

These results suggest that the UGT2B15 enzyme may have a role in the metabolism of dihydrotestosterone in prostate tissue and @GENE$ Asp85Tyr polymorphism is associated with @DISEASE$ risk.

[ "1" ]

636

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

[ "1" ]

637

The @GENE$ Asp allele may be a genetic risk factor for @DISEASE$, and might influence the course of Alzheimer disease, even though effects vary in different studies.

[ "0" ]

638

Our results strongly suggest that polymorphism in the @GENE$ promoter region might be associated with susceptibility to @DISEASE$.

[ "1" ]

639

This is the first report that demonstrates that the rare polymorphisms at codons 119 and 432 of @GENE$ gene have higher risk for endometrial cancer, and positive correlations with ERalpha and ERbeta expressions in @DISEASE$.

[ "1" ]

640

The study results suggest that the three @GENE$ gene polymorphisms are unlikely to be major genetic susceptibility factors for @DISEASE$ in the northern Han Chinese population.

[ "0" ]

641

We found evidence for association between @GENE$ and COGA @DISEASE$, history of blackouts, age at first drunkenness, and level of response to alcohol.

[ "1" ]

642

The lack of association between @GENE$ genotypes and IgE as well as atopic outcomes in this large German study population seems to indicate that CD14 genotypes may not directly be involved in the development of @DISEASE$ during childhood.

[ "0" ]

643

These results support the hypothesis that the Sl2 allele and, possibly, the @GENE$ allele evolved in the context of @DISEASE$ transmission and that in certain combinations probably confer a survival advantage on these populations.

[ "0" ]

644

Our results indicate that genetic polymorphisms affecting knee @DISEASE$ vary between populations (Japanese versus Caucasian) and sexes and indicate a role for @GENE$, COMP, FRZB, and COL2A1 in Caucasians.

[ "1" ]

645

For a similar level of exposure to established carcinogens, individuals with the @GENE$ A-allele genotypes appear to have a reduced risk of @DISEASE$.

[ "1" ]

646

Our findings do not indicate a role for the @GENE$ T-C polymorphism in @DISEASE$, but a role in male carriers of a BRCA2 mutation could not be excluded because of the small sample size.

[ "0" ]

647

The @GENE$ gene polymorphism, especially an increase in the frequency of the L allele, was found to be associated with @DISEASE$.

[ "0" ]

648

These data suggest that @GENE$ 82S upregulates the @DISEASE$ upon engagement of S100/calgranulins, and, thereby, may contribute to enhanced proinflammatory mechanisms in immune/inflammatory diseases.

[ "0" ]

649

The Bst U I polymorphism of the @GENE$ gene is a suitable genetic marker of @DISEASE$ but cannot be used in the prediction of the outcome of patients who have received hormonal therapy.

[ "1" ]

650

The Pro/Pro genotype of @GENE$ codon 72 appears to be an independent prognostic marker in @DISEASE$ patients.

[ "1" ]

651

We conclude that a different distribution of BMI could influence the results of analyses of @GENE$ gene polymorphisms in @DISEASE$-control studies.

[ "0" ]

652

The strong @DISEASE$ predisposition conferred by the @GENE$ and CFH SNPs may result from biological epistasis, because ERCC6 functions in universal transcription as a component of RNA pol I transcription complex.

[ "1" ]

653

@GENE$ 49 AA is protective from diabetes mellitus, whereas, CTLA-4 49 G allele (both as homozygotes and as heterozygotes ) confers an increased risk of @DISEASE$.

[ "1" ]

654

We conclude that APOE genotype influences the cellular distribution of increased reducible @GENE$ adduct accumulation in @DISEASE$.

[ "0" ]

655

Our results suggest MMP-2 and @GENE$ genotypes play a crucial role in gastric cancer invasion, but not with development of @DISEASE$.

[ "1" ]

656

The haplotype formed by 5 SNPs in the @GENE$ gene may be associated with type 2 diabetes in Han population of China, which is confirmed from statistics to be a susceptibility gene for the @DISEASE$.

[ "0" ]

657

A common variant of @GENE$, previously associated with a lower AHSG protein level, is thus more common among lean than obese and @DISEASE$ men, supporting the results from Ahsg knock-out mice, namely, that AHSG modulates body mass.

[ "0" ]

658

In conclusion, this is the first study to show that the @GENE$ T2854G variants are associated with elevated postprandial @DISEASE$ concentrations in the study population of Korean men.

[ "0" ]

659

The present findings indicated that certain alleles or genotypes of the @GENE$ gene may confer a susceptibility of @DISEASE$, especially of the hebephrenic type.

[ "1" ]

660

These data suggest a role for the @GENE$ I interferon pathway in resistance to @DISEASE$.

[ "0" ]

661

The current findings indicate that the IL-17F H161R variant influences the risk of asthma and is a natural IL-17F antagonist, suggesting a potential role for @GENE$ in the etiology of @DISEASE$.

[ "1" ]

662

Our results suggest a role of @GENE$ in the @DISEASE$ of CAL and might explain the excess of males affected with KD.

[ "0" ]

663

C311S polymorphism of @GENE$ has no significant correlation with @DISEASE$ in Han people of Chinese Hunan area and allele C/S is not an independent risk factor for stroke,neither is G148A.

[ "1" ]

664

The current study does not support the notion that the polymorphism in the @GENE$ gene constitutes a risk factor for either late-onset or early-onset @DISEASE$, which means that other genetic factors play a role in the development of AD in the Italian population.

[ "1" ]

665

The current results show that variation at the rs6295 polymorphism of the @GENE$ gene is not associated with @DISEASE$ generally.

[ "0" ]

666

Among postmenopausal Caucasian women, common variants of the @GENE$ gene are not associated with risk of @DISEASE$.

[ "1" ]

667

In our study, no correlation was detected between the polymorphism of @GENE$ gene and @DISEASE$.

[ "0" ]

668

The variant 180A>G (A60A) in @GENE$ is a risk factor for @DISEASE$, and a dynamic equilibrium of genes in HOX paralog 13 is involved in the pathogenesis of cryptorchidism.

[ "0" ]

669

The wild-@GENE$ allele of the TNF-alpha promoter polymorphism may be associated with mechanisms of @DISEASE$ sensitivity to inhaled SO2.

[ "0" ]

670

These data provide evidences for the contributions of exon2 and exon13 polymorphisms of @GENE$ to susceptibility to @DISEASE$ in Chinese Han population surrounding province.

[ "0" ]

671

PADI4 is significantly overexpressed in the blood of @DISEASE$ patients but genetic variation within @GENE$ is not a major risk factor for RA in Caucasians.

[ "1" ]

672

Together, our findings suggest that IL-1beta or @GENE$ gene polymorphisms may not be relevant in the susceptibility to @DISEASE$ or the clinical characteristics of Japanese patients with MS.

[ "0" ]

673

Genetic variations in @GENE$ or ADIPOR2 are unlikely to lead to a common genetic predisposition to insulin resistance or @DISEASE$ in the Japanese population.

[ "1" ]

674

demonstrated that neither single marker nor haplotype analysis revealed an association between variants at the @GENE$ locus and @DISEASE$, suggesting that it is unlikely that the GRIP1 polymorphisms investigated play a substantial role in conferring susceptibility to schizophrenia.

[ "1" ]

675

Thus, the @GENE$-1alpha gene locus influences carbohydrate metabolism and contributes to @DISEASE$ in the population studied.

[ "0" ]

676

The possible modifying effect on MBC risk in subjects carrying @GENE$/2 germ-line mutations of an occupation characterised by exposure to chemicals such as polycyclic aromatic hydrocarbons (PAH) that are capable of inducing @DISEASE$, may provide clues to the role of environmental exposures in modifying BC risk in mutation carriers in both genders.

[ "0" ]

677

Our data did not support the hypothesis that @GENE$ and/or MMP-3 gene promoter polymorphisms influenced the susceptibility to @DISEASE$ in Japanese patients, indicating MMP-1 and MMP-3 expressions were regulated by complex processes such as cytokine network in periodontal disease rather than gene polymorphisms.

[ "1" ]

678

These results suggest that a genetic polymorphism in the 5' flanking region of the @GENE$ gene would be associated with @DISEASE$ in lupus through modulating MCP-1 expression.

[ "0" ]

679

The @GENE$-232C > G polymorphism is not a major contributor to the pathogenesis of @DISEASE$ in the Danish population.

[ "1" ]

680

This report identifies a genetic association in humans between @DISEASE$ and @GENE$ class II and III genes.

[ "0" ]

681

The @GENE$ polymorphisms studied do not contribute to @DISEASE$ susceptibility in Japanese or Dutch sarcoidosis patients.

[ "0" ]

682

The @GENE$ C2 variant did not confer a risk for @DISEASE$ in Koreans.

[ "1" ]

683

If confirmed by others, our results indicate that more intensive @DISEASE$ prophylaxis is needed for patients with at least one @GENE$ G allele, possibly directed toward blunting early host cell production of IL-2.

[ "1" ]

684

In conclusion, alterations in the @GENE$ gene are unlikely to contribute importantly to the pathogenesis of @DISEASE$ or lipoatrophic diabetes mellitus in Japan.

[ "1" ]

685

@GENE$ germline genetic variation affects @DISEASE$ susceptibility, and possibly survival, in PMF, regardless of VF mutational status.

[ "0" ]

686

We conclude that genetic variants at the @GENE$ locus occur commonly in subjects with this @DISEASE$ (four out of 18 subjects with probably functional mutants) and may affect the individual's response to obesity and diabetes mellitus for the development of lipaemia.

[ "0" ]

687

Our results suggest that the G908R mutation of the CARD15/NOD2 gene, as well as the T allele and TT genotype of the @GENE$ promoter are associated with increased susceptibility for developing @DISEASE$.

[ "1" ]

688

The results suggest that the investigated BDNF polymorphisms are neither robust genetic risk factors nor determinants of @GENE$ protein levels in @DISEASE$.

[ "1" ]

689

the Gilbert @GENE$ allele increases the risk of @DISEASE$ formation in CF.

[ "1" ]

690

The @GENE$ genotype is an important genetic marker predicting an individual's predisposition to @DISEASE$.

[ "1" ]

691

Replication of the original @GENE$ findings in these 4 additional @DISEASE$ populations suggests that this gene (and perhaps others that interact with it) is important in the development and pathogenesis of asthma.

[ "1" ]

692

This study provides further evidence that sequence variation in @GENE$ is associated with an increased risk of breast cancer, and implies that @DISEASE$ in association with CHEK2 mutations does not involve loss of the wild type allele.

[ "0" ]

693

This new marker may provide a valuable tool to assess the risk for @GENE$-associated @DISEASE$, but it does not appear to be associated with asthma and/or atopy.

[ "0" ]

694

In the present study, we found that short polymorphic genotypes of [TTTA]n repeats of the @GENE$ gene were associated with @DISEASE$ risk.

[ "0" ]

695

a genetic polymorphism links MPO expression to Alzheimer's risk, in that a higher expressing SpSp MPO genotype was associated with increased incidence of @DISEASE$ in females, and decreased incidence in males (@GENE$.006)

[ "0" ]

696

Our findings provide further support that @GENE$ is a modifying gene that plays a role in determining interindividual variability in the proclivity for outward and self-directed @DISEASE$ found in some schizophrenic patients.

[ "0" ]

697

In contrast to other PPIs, esomeprazole-induced healing of @DISEASE$ is unrelated to the CYP2C19 genotype, which can be explained by the metabolic shift toward the @GENE$-mediated pathway.

[ "0" ]

698

The present findings show that the preferential Th2-@GENE$ response to @DISEASE$ was associated with a poorer prognosis and suggest that polymorphisms of the IL-4Ralpha gene may serve as useful genetic markers for assessing the risk of the development and progression of RCC.

[ "0" ]

699

In this study population, the authors were unable to confirm that the polymorphism of @GENE$-adrenergic receptor gene is a crucial factor of the susceptibility to @DISEASE$ and a major genetic determinant of different clinical status.

[ "0" ]