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   1 re assigned paired TMEM154 haplotypes (i.e., diplotypes).                                            
     2 HTT allele-specific inactivation for a given diplotype.                                              
     3 es for subjects carrying the Delta19_G/i19_A diplotype.                                              
     4 ere successfully genotyped and assigned MBL2 diplotypes.                                             
     5 is revealed further differential risk of HLA diplotypes.                                             
     6 typed DNA from blood samples determined COMT diplotypes.                                             
  
  
     9 a marginally significant excess of the H1/H1 diplotype among patients with Parkinson's disease (PD), 
  
  
  
  
  
    15 erved a robust association between the H1/H1 diplotype and PD risk (odds ratio for H1/H1 vs H1/H2 and
    16 a significant (P = 0.04) interaction of COMT diplotype and time-varying stress showed that a postbase
  
  
  
  
    21 lation studies of case-parents triads, whose diplotypes are simulated on the basis of draws from the 
    22 sis showed that ADH5 and ADH6 genotypes, and diplotypes at ADH1A, ADH1B, ADH1C and ADH7 (minimal P = 
    23 egion (GSTT2-22q11.23) with haplotype and/or diplotypes, but not individual SNP alleles associated wi
    24 tion was limited to incident cases with COMT diplotypes coding for low-activity COMT, signifying impa
  
    26 rent CYP2A6 alleles, their numerous possible diplotype combinations and non-additive allele effects. 
    27 ent IPD (n = 12) for children with defective diplotypes compared with cases with a single episode (OR
  
    29 s block and interaction between two specific diplotypes covering this block multiplicatively increase
  
    31 iate analysis of the haplotype combinations (diplotypes) demonstrated that both whites (odds ratio, 0
    32 We identified numerous SNPs, haplotypes, and diplotypes (diploid pairs of haplotypes) within the OCA2
  
    34   Each data set consists of haplotype pairs (diplotypes) for 20 SNPs typed at equal 50-kb intervals i
  
    36 rsons with the high-risk SNP6 and SNP9 AC/AC diplotype had an increased risk of 3-fold [95% confidenc
    37 ts indicated that individuals with the H8-H8 diplotype had heavier body weights and faster growth rat
    38 ot found in subjects with high-activity COMT diplotypes (hazard ratio = 1.42; 95% confidence limits: 
    39 incidence in subjects with low-activity COMT diplotypes (hazard ratio = 2.35; 95% confidence limits: 
    40  samples of marker haplotypes, genotypes, or diplotypes in case-control studies in which the markers 
  
    42    A predictive model that translates CYP2A6 diplotype into a single continuous variable was previous
    43 IV in LC isolated from individuals with CCR5 diplotypes known to be associated with low, intermediate
  
    45 risk for meningitis than children with other diplotypes (odds ratio [OR], 0.85; 95% confidence interv
  
    47  DTR analysis showed that ADH5 genotypes and diplotypes of ADH1A, ADH1B, ADH7, and ALDH2 were associa
  
    49 haplotypes fit into two main clades and that diplotypes of these clades were marginally associated wi
  
  
  
    53 ims of Zhou et al. that neuropeptide Y (NPY) diplotype-predicted expression is correlated with trait 
    54  specific alleles, genotypes, haplotypes and diplotypes that were significantly associated with risk 
    55 t 2 and 16, respectively, when the number of diplotypes (the pair of haplotypes that compose the geno
  
  
  
  
  
    61 of markers and are applicable to haplotypes, diplotypes, whole-genome association or candidate region
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