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900 | 900 | it is unlikely that common variants in MLH1, MLH3, PMS1, MSH2, MSH3 and @GENE$ contribute significantly to @DISEASE$ susceptibility. | [
"1"
] |
901 | 901 | An original finding is the increased risk of @DISEASE$ and recurrence of pregnancy negative events, probably by modulating the maternal-fetal flow, in women homozygous for the eNOS 894T allele previously analyzed for the @GENE$ I/D polymorphism. | [
"1"
] |
902 | 902 | In conclusion, this study shows that Korean with specific polymorphism in @GENE$ are neither more susceptible to develop cervical cancer nor more vulnerable for @DISEASE$. | [
"0"
] |
903 | 903 | No association between the @GENE$ -94 @DISEASE$/delATTG promoter polymorphism or with other NF-kappaB complex SNP in patients with PsA from Newfoundland was observed. | [
"0"
] |
904 | 904 | @GENE$ is not likely to be a major susceptibility gene for @DISEASE$ in this Korean population. | [
"1"
] |
905 | 905 | We conclude that multiple haplotypes on the @GENE$ gene seem to confer a risk for developing @DISEASE$ in Caucasians. | [
"1"
] |
906 | 906 | Polymorphisms in the GPX-1 and @GENE$ genes are associated with an increased risk of @DISEASE$. | [
"1"
] |
907 | 907 | Since the SH2D2A protein modulates T cell activation, this may be a mechanism for how short @GENE$ alleles confer susceptibility to develop @DISEASE$. | [
"1"
] |
908 | 908 | This study suggests a positive association between synapsin II and @DISEASE$, implying that @GENE$ is involved in the etiology of schizophrenia. | [
"1"
] |
909 | 909 | @GENE$ and PVRL2 have little or no effect on the clinical outcome of @DISEASE$. | [
"1"
] |
910 | 910 | This study therefore suggest no major modifying role for the @GENE$ polymorphism in development of asbestos-associated @DISEASE$. | [
"0"
] |
911 | 911 | (1) DRB1 * 0405 and DRB1 * 15 are closely associated with the susceptibility to VKH syndrome, DRB1 * 0405 may be the major susceptible gene and DRB1 * 15 may be the minor; (2) DRB1 * 14 and DRB1 * 08 are negatively associated with the susceptibility to @DISEASE$, suggesting that they may be the resistant genes; (3) @GENE$ * 0405 is not related to the clinical features, incidence of ocular complications as well as visual prognosis. | [
"1"
] |
912 | 912 | We conclude that variations in the nine ectodomains of @GENE$ do not increase susceptibility to @DISEASE$. | [
"1"
] |
913 | 913 | The results suggest that variation in @GENE$ affects risk of @DISEASE$ in the mestizo population of central Mexico (Mexico City and Orizaba) and in Mexican Americans (Starr County, Texas). | [
"1"
] |
914 | 914 | We conclude that @GENE$ through its K-variant, rather than a nearby marker, is a susceptibility factor for @DISEASE$ and enhances the AD risk defined by APOE epsilon4 alone in an age-dependent manner. | [
"0"
] |
915 | 915 | Our study finds no evidence for association of the @GENE$ SNP309 polymorphism with clinicopathologic variables, recurrence risk, and overall survival outcome in @DISEASE$. | [
"1"
] |
916 | 916 | Considering the relatively low frequency of haplotype 221 and that none of the haplotypes including 221 was associated with any of the @DISEASE$-related quantitative @GENE$ tested, it is concluded that SNP-43, -56, and -63 of the CAPN10 gene variants may play a limited role in the risk of type 2 diabetes risks in this cohort of West Africans. | [
"0"
] |
917 | 917 | The hybridization @GENE$ genotype at the site of 2257 in EXON2 of insulin-receptor gene might have a candidate gene to serve as a protective factor for @DISEASE$. | [
"0"
] |
918 | 918 | Although the polymorphism of @GENE$ gene G894T did not seem to play an important and direct role in the @DISEASE$ of EH it might have indirect effects through certain risk factors. | [
"0"
] |
919 | 919 | These results suggest that polymorphisms of the @GENE$ gene, but not the ACE gene, may be associated with the development of @DISEASE$. | [
"1"
] |
920 | 920 | Although linkage disequilibrium with other genetic alterations cannot be excluded, the @GENE$ core promoter variants, found in this study, may contribute to a common pathophysiologic feature of @DISEASE$. | [
"1"
] |
921 | 921 | The @GENE$ Thr92Ala variant does not confer an increased risk of T2D, @DISEASE$, or insulin resistance. | [
"0"
] |
922 | 922 | These findings suggest that the presence of the variant allele in the promoter of MMP2 or @GENE$ may be a protective factor for the development of @DISEASE$. | [
"1"
] |
923 | 923 | In conclusion, the @GENE$ blood group B allele was found to be an independent risk factor for @DISEASE$. | [
"1"
] |
924 | 924 | The C allele in the @GENE$ gene might be associated with the susceptibility to CAD and potentially plays an important role in the manifestation of @DISEASE$ among Chinese. | [
"1"
] |
925 | 925 | Despite the limited study sample, our data suggest that @GENE$ mutations might be present less frequently than KRAS mutations in Greek patients with @DISEASE$. | [
"0"
] |
926 | 926 | These results support the hypothesis that the African-American population is an older population compared with the other samples and the two @GENE$ receptors may play a role in @DISEASE$ pressure regulation. | [
"0"
] |
927 | 927 | Our results do not provide evidence for a strong involvement of @GENE$ in the development of AGA, although a @DISEASE$ role cannot be fully excluded. | [
"0"
] |
928 | 928 | These data suggest that the @GENE$ allele is more frequent in brain @DISEASE$ associated with large-vessel occlusion. | [
"0"
] |
929 | 929 | Neither @GENE$ I/D nor CYP11B2 -344C/T polymorphisms were useful to predict left ventricular mass, function or @DISEASE$ in our hypertensive patients with normal coronary arteries. | [
"0"
] |
930 | 930 | Our findings are consistent with the notion that genetic variation in the @GENE$ neurotransmitter system contributes to the @DISEASE$ of panic disorder. | [
"0"
] |
931 | 931 | These results indicate a possible association between the @GENE$ allele and an overexpression of noncognitive @DISEASE$ in AD. | [
"0"
] |
932 | 932 | Overtransmission of particular haplotypes of @GENE$, that may relate to the expression level of NrCAM in the brain, appeared to be associated with @DISEASE$ in the severe obsessive-compulsive behavior subset. | [
"0"
] |
933 | 933 | Our investigation suggests that the two promoter SNPs are unrelated to the development of @DISEASE$, however, further investigation at the promoter region of @GENE$ may be necessary to address its potential implication of gene expression in AD. | [
"1"
] |
934 | 934 | TT genotype of @GENE$-1055 is not an independent factor for COPD in Chinese Han people in Beijing, but increases the risk for smokers to develop @DISEASE$ and the one who has COPD family history as well. | [
"1"
] |
935 | 935 | We conclude from our data that @GENE$ does not play a major role in the development of @DISEASE$ in our Caucasian population. | [
"1"
] |
936 | 936 | The present study provides further evidence in support of the @GENE$ association with @DISEASE$ in Chinese population. | [
"1"
] |
937 | 937 | These observations suggest that lower expression of @GENE$ decreases the risk of @DISEASE$ by reducing the excretion of 2-hydroxyestradiol, the antiproliferative metabolite of E(2), in the endometrium. | [
"1"
] |
938 | 938 | This @DISEASE$ supports our hypothesis that a dominant gene within the @GENE$ region (marked by HSP70-1 and HSP70-2), but not necessarily HLA, is associated with CA in two different ethnic groups. | [
"0"
] |
939 | 939 | The present data indicate that mutations of @GENE$ may cause non-syndromic hearing @DISEASE$. | [
"0"
] |
940 | 940 | Although some molecular variants within the SLC3A1 gene were associated with clinical traits in @DISEASE$ patients, the low detection rate of mutations in this gene strongly suggests that variation of the @GENE$ is not the major genetic factor contributing to cystinuria in this Mediterranean population. | [
"1"
] |
941 | 941 | @GENE$ therapy reduces increased stent @DISEASE$ rates and improves clinical outcome following coronary stent implantation in patients bearing the Pl(A2)allele, suggesting that statins interfere with the functional consequence of a genetically determined platelet-mediated risk factor associated with Pl(A2)polymorphism. | [
"0"
] |
942 | 942 | C311S polymorphism of @GENE$ has no significant correlation with stroke in Han people of Chinese Hunan area and allele C/S is not an independent risk factor for @DISEASE$,neither is G148A. | [
"1"
] |
943 | 943 | In conclusion, a significant association between @DISEASE$ and @GENE$ T51C polymorphism localized on chromosome 3p21 was found. | [
"1"
] |
944 | 944 | These data suggest that there is a significant association between the genetic polymorphisms of @GENE$, p21, and specific combinations of the at-risk genotypes of these genes and the risk of developing @DISEASE$ in Korean women. | [
"1"
] |
945 | 945 | These results, in accordance with similar findings previously obtained in other ethnic groups, suggest that these two @GENE$ allelic variants may not have a direct role in the @DISEASE$ and development of obesity. | [
"0"
] |
946 | 946 | The SNP021 in the gene SCN7A is associated with essential hypertension of Chinese Han population in Shanghai and the role of @GENE$ gene in @DISEASE$ deserves to be further analyzed. | [
"1"
] |
947 | 947 | Our findings suggest that the (CCTTT)(n) repeat polymorphism in the promoter of the @GENE$ gene that affects promoter activity is a risk factor for the development of @DISEASE$, and this genetic effect seems independent of asthma. | [
"1"
] |
948 | 948 | These results indicate that polymorphisms in the @GENE$ gene are associated with NTG and may be a marker for the @DISEASE$. | [
"0"
] |
949 | 949 | These results suggest that in men, the human @GENE$ gene is associated with reduced amount of @DISEASE$ and lower insulin secretory responses to a glucose load. | [
"0"
] |
950 | 950 | Our data indicate polymorphism in intron 4 of the @GENE$ gene affects the occurrence of APA and may slightly modify the risk of sporadic @DISEASE$. | [
"1"
] |
951 | 951 | The @GENE$-V/F158 polymorphism has a significant impact on the development of @DISEASE$. | [
"0"
] |
952 | 952 | These findings suggest that the investigated @GENE$ genetic polymorphism does not play a major role in the pathogenesis of @DISEASE$. | [
"1"
] |
953 | 953 | These findings provide initial evidence that environmental risks as described by the Rutter Family Adversity Index moderate the impact of the @GENE$ gene on @DISEASE$ symptoms, suggesting a DAT1 effect only in those individuals exposed to psychosocial adversity. | [
"1"
] |
954 | 954 | Our findings suggest that these common @GENE$ polymorphisms do not play a major role in susceptibility to @DISEASE$ or type 2 diabetes in this population. | [
"0"
] |
955 | 955 | After correction for multiple comparisons, the addition of genetic information observed in the present study had little @GENE$ on risk prediction models for @DISEASE$. | [
"0"
] |
956 | 956 | The @GENE$ promoter SNP309 is associated with the presence of @DISEASE$ in Chinese patients especially those with H. | [
"0"
] |
957 | 957 | The polymorphism that confers susceptibility to @GENE$ II (@DISEASE$ in some populations is associated in United Kingdom Caucasians with enhanced microvascular function in the presence of normoglycaemia. | [
"0"
] |
958 | 958 | Our data suggest that neither the +36 TNFRSF1A SNP nor the +196 @GENE$ SNP is associated with @DISEASE$ severity in a population of Caucasian patients with RA. | [
"1"
] |
959 | 959 | These results suggested that the CTLA-4 gene might be involved in the susceptibility to @DISEASE$ in the Chinese Han population and both +49 and CT60 of @GENE$ gene might be the causal variants in RA disease. | [
"1"
] |
960 | 960 | We conclude, therefore, that the @GENE$-bp @DISEASE$ of the AIRE1 gene is not a susceptibility locus for the more common autoimmune endocrinopathies in the United Kingdom. | [
"0"
] |
961 | 961 | Our results show that the C1773 @DISEASE$ of @GENE$ increases susceptibility to hypertension, but not via hypercholesterolaemia. | [
"0"
] |
962 | 962 | Neither the @GENE$ K121Q nor the GLUT-1 XbaI polymorphism contribute to the genetic susceptibility of diabetic microvascular @DISEASE$ in Danish type 1 diabetic patients. | [
"0"
] |
963 | 963 | this large-scale evaluation of candidate @DISEASE$ genes has identified common genetic variants in the regulatory regions of @GENE$ that could be associated with bladder cancer risk. | [
"0"
] |
964 | 964 | These data suggest that there is a significant association between the genetic polymorphisms of p53, @GENE$, and specific combinations of the at-risk genotypes of these genes and the risk of developing @DISEASE$ in Korean women. | [
"0"
] |
965 | 965 | An original @DISEASE$ is the increased risk of pre-eclampsia and recurrence of pregnancy negative events, probably by modulating the maternal-fetal flow, in women homozygous for the @GENE$ 894T allele previously analyzed for the ACE I/D polymorphism. | [
"0"
] |
966 | 966 | These results indicate that the @GENE$ variant haplotype is functionally significant in patients with @DISEASE$, being associated with increased nuclear translocation of NF-kappaB, more severe organ dysfunction, and higher mortality. | [
"1"
] |
967 | 967 | None of the SNPs of KCNQ1 P448R, KCNQ1 R519H, KCNQ1 G643S, KCNE1 G38S and @GENE$ D85N was associated with @DISEASE$ phenotype, but KCNE4 E145D may relation to atrial fibrillation. | [
"1"
] |
968 | 968 | In conclusion, TSER genotype is not an efficacious marker for @DISEASE$ sensitivity to 5-@GENE$-based oral adjuvant chemotherapy for Japanese colorectal cancer patients after curative resection. | [
"0"
] |
969 | 969 | These results indicated that @GENE$ polymorphisms may be associated with the level of blood IGFBP-3 protein and an increased risk of @DISEASE$. | [
"1"
] |
970 | 970 | Our data support the hypothesis that the @GENE$ locus may be a significant genetic determinant for @DISEASE$ risk in whites and that women are more sensitive to the genetic effects of perilipin than men. | [
"1"
] |
971 | 971 | Mutations in the @GENE$ gene are unlikely to be directly causative of @DISEASE$. | [
"1"
] |
972 | 972 | @DISEASE$, serum folate levels and both C677T and A1298C @GENE$ mutations are associated with CVD in HD patients. | [
"0"
] |
973 | 973 | @GENE$ activation is present in healthy subjects at risk of developing @DISEASE$ as well as in established type 2 diabetic patients, and it is associated with impairments in the vascular reactivity in the skin microcirculation. | [
"0"
] |
974 | 974 | The investigated @GENE$ and 5-@DISEASE$-2A gene variants, therefore, do not seem to play a major role in SSRI antidepressant activity. | [
"0"
] |
975 | 975 | Based on these data, @GENE$ is not the causative gene for @DISEASE$. | [
"1"
] |
976 | 976 | This study suggests that possession of the @GENE$ allele with higher levels of IFN-alpha significantly increases the risk of @DISEASE$. | [
"0"
] |
977 | 977 | None of the SNPs of KCNQ1 P448R, KCNQ1 R519H, KCNQ1 G643S, KCNE1 G38S and @GENE$ D85N was associated with atrial fibrillation phenotype, but KCNE4 E145D may relation to @DISEASE$. | [
"1"
] |
978 | 978 | We conclude that IL-4-589*T, but not TNF-alpha-308*2 or Fcalpha RIbeta*G, is a risk factor for the development of @GENE$, @DISEASE$, and rhinitis by 12 mo of age. | [
"1"
] |
979 | 979 | These data provide no evidence that heteroallelic mutations or polymorphisms in the @GENE$ are involved in the development of @DISEASE$ early-onset MG but raise issues for future studies. | [
"0"
] |
980 | 980 | FAS and @GENE$ polymorphisms appear to jointly contribute to risk of @DISEASE$ in this southern Chinese population. | [
"1"
] |
981 | 981 | The areas of atherosclerotic lesions in @GENE$ appear to be dependent on the amount of alcohol @DISEASE$, especially in men carrying the PON1 M55 allele. | [
"0"
] |
982 | 982 | The present findings indicated that certain alleles or genotypes of the CNR1 gene may confer a susceptibility of @DISEASE$, especially of the hebephrenic @GENE$. | [
"0"
] |
983 | 983 | Consequently, the @DISEASE$ suggests that the @GENE$ polymorphism was not associated with the risk of myeloid leukemia. | [
"0"
] |
984 | 984 | Our results show that the 4G/4G PAI-1 genotype appears to be associated with an elevated relative risk of developing @DISEASE$, regardless of @GENE$ levels and other hypertension-related factors, in a representative sample of the Spanish population. | [
"1"
] |
985 | 985 | The @GENE$ variant at position -308 in the promoter region of the TNFalpha gene does not influence the amount of weight lost in @DISEASE$ and obese men and women on a 30% energy restricted diet. | [
"0"
] |
986 | 986 | the 660L allele may be associated with a moderately increased risk of breast cancer, but that other common SNPs in the @GENE$ gene are unlikely to be associated with a substantial risk of @DISEASE$. | [
"1"
] |
987 | 987 | These findings suggest that a variant in @GENE$ is not only important in the development of @DISEASE$ but also in disease progression, possibly related to enhanced airway remodelling. | [
"1"
] |
988 | 988 | Our results suggest @GENE$ and TIMP-2 genotypes play a crucial role in @DISEASE$ invasion, but not with development of gastric cancer. | [
"1"
] |
989 | 989 | These results show no evidence of an association between the @GENE$-uVNTR polymorphism and completed suicides and suggest that MAOA is not involved in the susceptibility to @DISEASE$. | [
"1"
] |
990 | 990 | These findings suggest that individual susceptibility of @DISEASE$ may be modulated by @GENE$ and MnSOD polymorphisms, and that the combination of genetic factors involved in oxidative stress response with environmental carcinogens may play an important role in bladder carcinogenesis. | [
"1"
] |
991 | 991 | These data suggest that this polymorphism of the @GENE$ gene is not associated with GD in the UK and is therefore not contributing to @DISEASE$ susceptibility in the chromosomal region designated GD-2. | [
"0"
] |
992 | 992 | Our results suggest that the @GENE$ Val511Ala SNP does not antagonize the effect of NSAIDs on colon cancer risk and provides support that NSAID use and the COX-2 Val511Ala SNP may contribute to a reduced risk of @DISEASE$ among African Americans. | [
"1"
] |
993 | 993 | Together, our findings suggest that the presence of @GENE$ gene polymorphisms may be inconclusive in the susceptibility to @DISEASE$ or in the clinical characteristics of Japanese patients with MS and, therefore, need further studies. | [
"1"
] |
994 | 994 | These results suggest that variation of @GENE$ may be an important determinant of @DISEASE$, in part through the mechanism of accelerated postmenopausal bone loss. | [
"0"
] |
995 | 995 | We conclude that @GENE$ (-174) polymorphism does not influence the risk of developing @DISEASE$ in our cohort. | [
"1"
] |
996 | 996 | Our results indicate for the first time that low numbers of @GENE$) PNTR and plasma Lp(a) levels are independently associated with both ischemic and @DISEASE$ in Chinese. | [
"0"
] |
997 | 997 | In conclusion, differences in estrogen levels due to polymorphism at the @GENE$ CYP19 gene may predispose men to increased @DISEASE$ and fracture risk. | [
"0"
] |
998 | 998 | (1) @GENE$ * 0405 and DRB1 * 15 are closely associated with the susceptibility to VKH syndrome, DRB1 * 0405 may be the major susceptible gene and DRB1 * 15 may be the minor; (2) DRB1 * 14 and DRB1 * 08 are negatively associated with the susceptibility to @DISEASE$, suggesting that they may be the resistant genes; (3) DRB1 * 0405 is not related to the clinical features, incidence of ocular complications as well as visual prognosis. | [
"1"
] |
999 | 999 | These two @GENE$ gene mutations may account for a substantial fraction of hereditary @DISEASE$. | [
"1"
] |