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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"
] |