1Mette Christiansen, Betina Samuelsen, Samuelsen B, et al. Correlation between serology and genetics of weak D types in Denmark. Transfusion ,2008,48 ( 1 ) : 187-193.
2Avent ND, Martin PG, Armsrong-Fisher SS, ct al. Evidence of genetic diversity underlying RhD-, weak D( D^u), and partial D phenotypes as determined by multiplex polymerase chain reaction analysis of the RHD gene. Blood, 1997,89 (7) :2568-2577.
3Huang CH. Molecular insights into the Rh protein family and associated antigens . Curr Opin Hematol, 1997,4 ( 2 ) :94-103.
4Franz F. Wanger,Christoph Gassner,Thomas H. et al. Molecular Basis of Weak D Phenotypes. Blood,1999,93( 1 ) :385-393.
5Wagner FF, Frohmajer A, Ladewig B, et al. Weak D allele express distinct phenotypes. Blood ,2000,95 ( 8 ) :2699-2708.
7Legler TJ,Maas JH,Kohler M,et al. RHD sequencing: a new tool for decision making on transfusion therapy and provision of Rh prophylaxis. Transfus Med,2001,11(5) :383.
8Wagner FF,Gassner C, Muller TH, et al. Molecular basis of weak D phenotypes. Blood, 1999,93( 1 ) ~ 385.
9Legler TJ, Wiemann V, Ohto H, et al. D(Va) category phenotype and genotype in Japanese families. Vox Sang,2000,78(3) : 194.
10Chang JG,Wang JC, Yang TY,et al. Human RhD^el is caused by a deletion of 1,013 bp between introns 8 and 9 including exon 9 of RHD gene.Blood, 1998,92(7) :2602.
5Avent DN,Reid EM. The P,h blood group system:a review. Blood, 2000,95 ( 2 ) :375-387.
6Avent N D, Martin P G, Armstrong Fisher SS, et al. Evidence of ge- neticdiversity underlying RhD-,weak D(Du) ,and partialD pheno- typesas determined by multiplex polymerase chain reaction analys- isof the RhD gene. Blood,1997,89(7) : 2568-2577.
7C heft -f Zahar B, Bony V, S teffensen R, eta l. Shift from Rh-pos- it ive to Rh-n egat ive phenotype caused by a somatic mu tat ion w ithinth eRHD gene in a patient with ehron icm yeloeytie leukaemi- a. B r JH aematol,1998,102(8) : 1263-1270.