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1 encies and r(2) from diploid genotypes under Hardy-Weinberg Equilibrium.
2 t RHO c.68C>A, (p.P23H) was calculated using Hardy-Weinberg equilibrium.
3 he allele distribution was inconsistent with Hardy-Weinberg equilibrium.
4                  All control samples were in Hardy-Weinberg equilibrium.
5 ously and did not deviate significantly from Hardy-Weinberg equilibrium.
6 e distribution of all 5 polymorphisms was in Hardy-Weinberg equilibrium.
7 H depletes heterozygotes, thereby disrupting Hardy-Weinberg equilibrium.
8 lex survey designs to assess deviations from Hardy-Weinberg equilibrium.
9 cus in a population, under the assumption of Hardy-Weinberg equilibrium.
10                             All SNPs were in Hardy-Weinberg equilibrium.
11              The three polymorphisms were in Hardy-Weinberg equilibrium.
12 ty of allele frequencies in the sexes assume Hardy-Weinberg equilibrium.
13 nonequilibrium population that deviates from Hardy-Weinberg equilibrium.
14 ere observed in both populations and were in Hardy-Weinberg equilibrium.
15 type frequencies deviated significantly from Hardy-Weinberg equilibrium.
16 ism, perfectly matched the expectation under Hardy-Weinberg equilibrium.
17 es in the study population were assessed for Hardy-Weinberg equilibrium.
18    All observed genotype frequencies were in Hardy-Weinberg equilibrium.
19  in the general population than predicted by Hardy-Weinberg Equilibrium.
20 ns, and frequencies of genotypes were in the Hardy-Weinberg equilibrium.
21 re randomly sampled from a population not in Hardy-Weinberg equilibrium.
22 duplication were present in concordance with Hardy-Weinberg equilibrium (13% and 23%, respectively),
23  homogeneity is known to be valid only under Hardy-Weinberg equilibrium, a property that may not hold
24 ease be done on the basis of deviations from Hardy-Weinberg equilibrium among affected individuals.
25  States Caucasian random blood donors was in Hardy-Weinberg equilibrium and CCR5Delta32 homozygotes r
26 PNPLA3 and TM6SF2 polymorphisms conformed to Hardy-Weinberg equilibrium and did not associate with fi
27 o STR locus was observed to deviate from the Hardy-Weinberg equilibrium and linkage disequilibriums a
28  met stringent criteria for concordance with Hardy-Weinberg equilibrium and low genotyping error rate
29 by describing theoretical expectations under Hardy-Weinberg Equilibrium and provide recommendations f
30    The PTPN2 variant rs2542151 deviated from Hardy-Weinberg equilibrium and was excluded from analyse
31                           SNPs that followed Hardy-Weinberg equilibrium and yielded >/= 95% genotypin
32 equency, genotype frequency, heterozygosity, Hardy-Weinberg equilibrium, and linkage disequilibrium (
33 iteria for missing genotypes, departure from Hardy-Weinberg equilibrium, and low minor allele frequen
34 xcess of homozygotes, over that predicted by Hardy-Weinberg equilibrium; and (3) the model-predicted
35 ality control (QC) tests, including tests of Hardy-Weinberg equilibrium, are not sensitive enough to
36               Standard statistical tests for Hardy-Weinberg equilibrium assume the equality of allele
37 vironment independence assumption and 4) the Hardy-Weinberg equilibrium assumption.
38 res on population genetics to illustrate the Hardy-Weinberg equilibrium, calculate allele frequencies
39                     However, deviations from Hardy-Weinberg Equilibrium can inflate the chance of a f
40 sm available in a breeding program is not in Hardy-Weinberg equilibrium, classical concepts that assu
41 dies have explored the use of departure from Hardy-Weinberg equilibrium (DHW) for fine mapping Mendel
42 ntist approach that is appropriate even when Hardy-Weinberg equilibrium does not hold.
43 he markers showed significant deviation from Hardy Weinberg equilibrium except for HLD88 locus and no
44  per subpopulation as well as calculation of Hardy-Weinberg equilibrium for each subpopulation.
45                 Bayesian test procedures for Hardy-Weinberg equilibrium for the autosomes have been d
46  Recently, frequentist statistical tests for Hardy-Weinberg equilibrium have been proposed specifical
47 eral instances of significant deviation from Hardy Weinberg Equilibrium (HWE).
48 viduals with SNS, we observed deviation from Hardy-Weinberg Equilibrium (HWE) (p = 0.012) for p.Val44
49 es, e.g. STRUCTURE and L-POP, usually assume Hardy-Weinberg equilibrium (HWE) and linkage equilibrium
50 g allele frequencies using the assumption of Hardy-Weinberg equilibrium (HWE) as a prior.
51                                          The Hardy-Weinberg equilibrium (HWE) assumption is essential
52     We explore the extent of deviations from Hardy-Weinberg equilibrium (HWE) at a marker locus and l
53                              Deviations from Hardy-Weinberg equilibrium (HWE) can indicate inbreeding
54                  Testing for deviations from Hardy-Weinberg equilibrium (HWE) can provide fundamental
55 upported by a significant deviation from the Hardy-Weinberg equilibrium (HWE) due to a deficiency of
56 th newborns of first-time mothers outside of Hardy-Weinberg equilibrium (HWE) during peak PM season.
57 ypotheses that could explain deviations from Hardy-Weinberg equilibrium (HWE) expectations due to het
58 al and per subpopulation, and calculation of Hardy-Weinberg Equilibrium (HWE) for each subpopulation.
59  Genotype distributions for all SNPs were in Hardy-Weinberg equilibrium (HWE) in controls, but in cas
60                                  To test for Hardy-Weinberg Equilibrium (HWE) in NGHS, two test stati
61 SCN4A commonly shows extreme deviations from Hardy-Weinberg equilibrium (HWE) in these populations, w
62 e performing association analyses, assessing Hardy-Weinberg equilibrium (HWE) is a crucial step in qu
63                  Testing genetic markers for Hardy-Weinberg equilibrium (HWE) is an important tool fo
64                                              Hardy-Weinberg equilibrium (HWE) is often employed to te
65                    Detecting departures from Hardy-Weinberg equilibrium (HWE) of marker-genotype freq
66 viation of a single homozygous genotype from Hardy-Weinberg equilibrium (HWE) proportion.
67 tween markers and disease were analyzed by a Hardy-Weinberg equilibrium (HWE) test, a conventional ca
68 -genome case-control association studies and Hardy-Weinberg equilibrium (HWE) testing for data qualit
69 endence between pairs of alleles at a locus, Hardy-Weinberg equilibrium (HWE), is presented.
70                 In populations conforming to Hardy-Weinberg equilibrium (HWE), screening for unreliab
71 e likelihood incorporating the assumption of Hardy-Weinberg equilibrium (HWE).
72 18) and -137 (G-->C) (rs187238), were not in Hardy-Weinberg equilibrium (HWE).
73                       This variant is not in Hardy-Weinberg equilibrium (HWE).
74  APO, ESR1 and PV92 loci were found to be in Hardy-Weinberg equilibrium in all the ethnic groups, whi
75               All of the six markers were in Hardy-Weinberg equilibrium in controls, but SNP3 (rs1824
76             All markers were consistent with Hardy-Weinberg equilibrium in controls, but some markers
77 gote deficiency in females but which were in Hardy-Weinberg equilibrium in males, consistent with deg
78                  Testing for deviations from Hardy-Weinberg equilibrium is a widely recommended pract
79 lid method that corrects for deviations from Hardy-Weinberg Equilibrium is presented, so that the cha
80 he authors assume Mendelian inheritance, but Hardy-Weinberg equilibrium is unnecessary.
81 ype frequency distributions, deviations from Hardy-Weinberg equilibrium, linkage disequilibrium, and
82 t-guided filters based on QC variables [e.g. Hardy-Weinberg equilibrium, missing proportion (MSP) and
83 ribution of HbSS and HbSC genotypes assuming Hardy-Weinberg equilibrium near birth.
84                                              Hardy-Weinberg equilibrium need not be assumed.
85 kers were shown to exhibit no deviation from Hardy-Weinberg equilibrium, nor any linkage disequilibri
86 ition, our method relaxes the requirement of Hardy-Weinberg equilibrium of haplotype frequencies in c
87 he likelihood-ratio statistic, which assumes Hardy-Weinberg equilibrium of the marker phenotype propo
88 IM, incorporating chosen assumptions such as Hardy-Weinberg equilibrium or exchangeability of parenta
89  to estimate the risk ratio without assuming Hardy-Weinberg equilibrium or random mating.
90 ic factors, and it allows for deviation from Hardy-Weinberg equilibrium owing to inbreeding.
91  excess of common variation and deviate from Hardy-Weinberg equilibrium (p < 0.05), consistent with h
92  allele distribution strongly deviating from Hardy-Weinberg equilibrium, possibly implying selection
93 g Vieland and Huang's proof is that of joint Hardy-Weinberg equilibrium proportions at two trait loci
94 otypes in the general population comply with Hardy-Weinberg Equilibrium proportions, which may not al
95  similar to those previously observed and in Hardy-Weinberg equilibrium: SS 61.1%, Ss 36.2%, and ss 2
96 to approximate the discrete distributions of Hardy-Weinberg equilibrium test statistics and P-values.
97 trategies, more SNPs in GenoSNP may fail the Hardy-Weinberg Equilibrium test.
98                                              Hardy-Weinberg Equilibrium tests and the comparison of o
99 n this paper, the authors present a test for Hardy-Weinberg equilibrium that adjusts for the sample w
100         After accounting for deviations from Hardy-Weinberg equilibrium, the best-fitting model that
101 e show that it is robust to the violation of Hardy-Weinberg equilibrium, to the presence of missing d
102   After removing six loci that departed from Hardy-Weinberg equilibrium, we measured genetic variatio
103 homozygotes compared with that expected from Hardy-Weinberg equilibrium, whereas in males there is an
104 ives the first Bayesian approach for testing Hardy-Weinberg equilibrium with biallelic markers at the
105 pproximately 50% in the population and is in Hardy-Weinberg equilibrium with the intact allele.
106 , which could be partly explained by lack of Hardy-Weinberg equilibrium, with an excess of homozygote
107 ulation cohorts, this mutation deviated from Hardy-Weinberg equilibrium, with an overrepresentation o
108 ccomplished by eliminating the assumption of Hardy-Weinberg equilibrium within clusters and, instead,
109 cies of the parents showed no deviation from Hardy-Weinberg equilibrium within each cohort.

 
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