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Killexams : Hitachi Replication test contents - BingNews https://killexams.com/pass4sure/exam-detail/HH0-500 Search results Killexams : Hitachi Replication test contents - BingNews https://killexams.com/pass4sure/exam-detail/HH0-500 https://killexams.com/exam_list/Hitachi Killexams : A Genetic Risk Factor for Periodic Limb Movements in Sleep

Genomic Markers

Figure 1. Figure 1. Linkage Disequilibrium at the BTBD9 Locus.

The genomewide significant markers, rs3923809 and rs6923737, are located in a diffuse linkage-disequilibrium block overlapping portions of the BTB (POZ) domain–containing 9 (BTBD9) gene, the glyoxalase I (GLO1) gene, and markers in the promoter region of the dynein, axonemal, heavy polypeptide 8 (DNAH8) gene. The block is adjacent to the testis expressed sequence 27 (TEX27) gene. Data are from the single-nucleotide–polymorphism (SNP) International HapMap Project (release 19) of the Centre d'Etude du Polymorphisme Humain samples from Utah.

Table 1. Table 1. Association between Allele A of SNP rs3923809 and RLS with Periodic Leg Movements in Sleep among Subjects in Iceland and the United States.

To minimize phenotypic heterogeneity, we focused our initial genomewide association analysis on 306 subjects with RLS who also had periodic limb movements in sleep. Two markers, rs3923809 and rs6923737, in an intron of the BTB (POZ) domain–containing 9 (BTBD9) gene on chromosome 6p21.2 (Figure 1) showed genomewide associations that were significant (for rs3923809: odds ratio, 1.8; P=2×10–9; for rs6923737: odds ratio, 1.7; P=1×10–7) (Table 1, and Fig. 1 and Table 2 of the Supplementary Appendix). After adjustment for rs3923809, the association with rs6923737 was no longer significant (P=0.16), whereas the association with rs3923809 remained significant after adjustment for rs6923737 (P=0.001). None of the other 70 SNPs in a 600-kb region around rs3923809 remained significant after adjustments for rs3923809 and for multiple testing. The association with rs3923809 remained significant after adjustment for each of the SNPs individually (Table 2 of the Supplementary Appendix).

To validate these results, we analyzed a second Icelandic trial of 123 subjects with RLS and periodic limb movements in sleep and 1233 controls. The results with the second trial significantly replicated the original results for rs3923809 (odds ratio, 1.8; P=4×10–4) (Table 1, and Table 2 of the Supplementary Appendix). Extending the replication effort to a third trial of 188 subjects with RLS and periodic limb movements in sleep and 662 controls from the United States further confirmed the initial result for rs3923809 (odds ratio, 1.5; P=0.004) (Table 1). With all three samples combined, the association between the A allele of rs3923809 and RLS and periodic limb movements in sleep was highly significant (odds ratio, 1.7; P=3×10–14). There was no significant deviation from the multiplicative model, which assumed that the ratio of risk for homozygous carriers (AA) to heterozygous carriers (AG) was the same as the ratio of risk for heterozygous carriers to homozygous noncarriers (GG) in both the Icelandic subjects and the U.S. subjects (Table 3 of the Supplementary Appendix). The odds ratio for homozygous carriers was estimated at 3.2 for the Icelandic subjects and 2.3 for the U.S. subjects under the multiplicative model and at 4.3 for the Icelandic subjects and 2.0 for the U.S. subjects under the full model.

Table 2. Table 2. Association between Allele A of SNP rs3923809 and RLS with or without Periodic Leg Movements in Sleep among Subjects in Iceland.

Among the 229 subjects who reported having RLS symptoms in the absence of periodic limb movements (35%), there was no association with the A allele of rs3923809 (odds ratio, 1.0; P=0.81) (Table 2). Conversely, among the 105 subjects who had periodic limb movements in sleep but who did not meet the RLS consensus criteria, there was an association with the A allele of marker rs3923809 (odds ratio, 2.3; P=2×10–6) (Table 2). The odds ratio for this group did not differ significantly from that for the group that had RLS plus periodic limb movements in sleep (P=0.19). With the combined data from all the Icelandic subjects who had periodic limb movements in sleep (i.e., those with and those without RLS), the strength of the association (odds ratio, 1.9; P=1×10–17) was greater than that for the group with RLS plus periodic limb movements in sleep alone.

Figure 2. Figure 2. Correlation between the Frequency of Periodic Limb Movements in Sleep with the Presence of Allele A of Marker rs3923809 and of Homozygosity for the AA Genotype.

A total of 943 Icelandic subjects with RLS and their relatives were genotyped for marker rs3923809 and were evaluated for the frequency of periodic limb movements per hour of sleep. The subjects were then grouped into four categories on the basis of the frequency of limb movements, as follows: 271 subjects with 0 to 5 movements, 182 subjects with 6 to 10 movements, 212 subjects with 11 to 20 movements, and 278 subjects with 21 or more movements (Panel A, and data in the Supplementary Appendix). The odds ratio for having allele A of marker rs3923809 increased with the number of periodic limb movements, from 1.0 in the group with 5 or fewer movements to 2.0 in the group with 21 or more movements. Subjects were also grouped according to genotype into AA homozygotes (502 subjects), AG heterozygotes (371 subjects), and GG homozygotes (70 subjects) (Panel B). For marker rs3923809, the frequency of movements was greater in AA homozygotes than in AG heterozygotes (P=0.003) and greater in AG heterozygotes than in GG homozygotes (P<0.001). AA homozygotes moved nearly twice as often during each hour of sleep as did noncarriers (P<0.001). I bars indicate standard errors.

We found that the frequency of periodic limb movements in sleep correlated with the presence of allele A of marker rs3923809 (Figure 2A) and that AA homozygotes had almost twice as many limb movements per hour of sleep as did noncarriers (P<0.001) (Figure 2B). The odds ratio for the group of subjects with the most severe symptoms (>20 movements per hour of sleep) was 2.0, whereas it was 1.0 for the group with the least severe symptoms (≤5 movements per hour of sleep) (Figure 2A). No significant correlation was observed between allele A and the severity of RLS symptoms, as assessed on the basis of the IRLSSG rating scale (P=0.35) or the self-reported age at the onset of RLS symptoms (P=0.73).

Other Risk Factors

Female sex, advanced age, depletion of body iron stores, and western European ancestry were risk factors for RLS.38,39 To determine whether these factors interact with the at-risk variant, we analyzed them as covariates in conferring a risk of RLS. The risk of RLS and periodic limb movements in sleep conferred by allele A of rs3923809 in men was greater than that for women (odds ratio, 2.0 vs. 1.7), although the difference was not significant (P=0.28). A similarly insignificant trend was observed for the combined groups with periodic limb movements in sleep (odds ratio for men, 2.3; odds ratio for women, 1.7; P=0.09). The number of periodic limb movements in sleep was significantly higher after the age of 50 years than at a younger age (P<0.001 for both sexes), a finding that is consistent with a previous study.23 The difference was significantly less in women (P=0.04).

Figure 3. Figure 3. Serum Ferritin Levels in Subjects with RLS and Their Relatives.

Among 362 men (Panel A) and 603 women (Panel B), serum ferritin levels decreased by 13% per A allele at marker rs3923809 (95% CI, 5 to 20; P=0.002).

The principal clinical measures of iron availability are serum iron, transferrin iron-binding capacity, and ferritin. Serum soluble transferrin receptor, ferritin, total iron-binding capacity, and iron were assayed in 965 Icelandic subjects (subjects with RLS and their relatives). The ferritin index, a measure inversely related to body iron stores, was increased by 5.5% per A allele of marker rs3923809 (95% confidence interval [CI], 1 to 10; P=0.02). In line with this observation, serum ferritin levels were decreased by 13% per A allele (95% CI, 5 to 20; P=0.002) (Figure 3).

Wed, 20 Jul 2022 12:00:00 -0500 en text/html https://www.nejm.org/doi/10.1056/NEJMoa072743
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