Human Blood teams is a accomplished and entirely referenced textual content protecting medical and medical points of crimson cellphone floor antigens, including:
- molecular genetics
- biological functions
- clinical importance in transfusion medicine
Over a century has handed seeing that Landsteiner came upon the human blood teams, making the perform of blood transfusion attainable. but, within the six years because the first variation of Human Blood teams was once released, new blood teams were chanced on, a number of blood crew genes were cloned, and the molecular backgrounds of diverse blood crew versions were labored out. All this new details has made the creation of a moment version of Human Blood teams timely.
This e-book is an important reference resource for all these operating within the box of blood transfusion and blood banking.
Chapter 1 Human Blood teams: creation, Terminology, and serve as (pages 1–6):
Chapter 2 ABO, Hh, and Lewis platforms (pages 7–98):
Chapter three MNS Blood crew approach (pages 99–174):
Chapter four P Blood teams (pages 175–194):
Chapter five Rh Blood workforce approach (pages 195–274):
Chapter 6 Lutheran Blood team process (pages 275–294):
Chapter 7 Kell Blood team method (pages 295–323):
Chapter eight Duffy Blood workforce method (pages 324–341):
Chapter nine Kidd Blood workforce process (pages 342–351):
Chapter 10 Diego Blood crew process (pages 352–368):
Chapter eleven Yt Blood crew procedure (pages 369–373):
Chapter 12 Xg Blood team approach (pages 374–386):
Chapter thirteen Scianna Blood staff approach and the Radin Antigen (pages 387–391):
Chapter 14 Dombrock Blood staff process (pages 392–397):
Chapter 15 Colton Blood staff method (pages 398–403):
Chapter sixteen LW Blood team approach (pages 404–413):
Chapter 17 Chido/Rodgers Blood staff procedure (pages 414–425):
Chapter 18 Gerbich Blood staff approach (pages 426–443):
Chapter 19 Cromer Blood crew procedure (pages 444–454):
Chapter 20 Knops Blood staff process and the fee Antigens (pages 455–464):
Chapter 21 Indian Blood staff procedure and the An Wjantigen (pages 465–472):
Chapter 22 okay Blood crew method (pages 473–475):
Chapter 23 RAPH Blood staff method (pages 476–477):
Chapter 24 JMH Blood staff approach (pages 478–481):
Chapter 25 Ii Antigens and chilly Agglutination (pages 482–497):
Chapter 26 Er Antigens (pages 498–499):
Chapter 27 Low Frequency Antigens (pages 500–504):
Chapter 28 excessive Frequency Antigens (pages 505–513):
Chapter 29 Sid Antigens (pages 514–520):
Chapter 30 Human Leucocyte linked (HLA) category I Antigens on purple Cells (pages 521–523):
Chapter 31 Polyagglutination and Cryptantigens (pages 524–532):
Chapter 32 Blood team Gene Mapping (pages 533–548):
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Additional info for Human Blood Groups, Second Edition
The other sequences represent Japanese A1 and four A2 alleles, showing how they differ from the consensus sequence. Some silent nucleotide changes are not shown. 26 ABO, Hh, AND LEWIS SYSTEMS lectin , conversion of H sites with radiolabelled UDP-N-acetylgalactosamine and A-transferase [27,238,239], and ﬂow cytometry with monoclonal antibodies . Estimated numbers of antigens sites per red cell can be summarized as follows: A1 8–12 ¥ 105 A2 1–4 ¥ 105 A1B 5–9 ¥ 105 A2B 1 ¥ 105 [235–240,242,243].
However, after extended incubation with A2 enzyme, O cells may be weakly agglutinated by A1-speciﬁc reagents . A1 enzyme can convert A2 cells to A1 phenotype [226,227]. N-acetylgalactosaminyltransferases from 25 CHAPTER 2 A1 and A2 sources have the same speciﬁcity for low molecular weight acceptors and both synthesize the same A determinant . 5, activity of Atransferase from A1 serum, with low molecular weight substrate, is 5–10 times higher than that from A2 serum . Schachter et al.
290] sequenced exons, splice sites, and promoter regions of the ABO genes from other individuals with weak A antigens. 17). Three were A2 alleles (Pro156Leu and the C1060 deletion) with additional missense mutations. In Aw-3 the mutation encoding Arg68Thr is in exon 4 and in Aw-2 the mutation encoding Gly177Ala is in exon 6. These are the only missense mutations associated with a weak subgroup outside exon 7. The other two (Aw-4 and -5) are A1 alleles with an additional exon 7 missense mutation.