10949nam 2200601 a 450 991081368500332120240313151437.01-118-49359-11-299-24140-91-118-49362-1(CKB)2560000000098534(EBL)1129724(SSID)ssj0000831563(PQKBManifestationID)12410290(PQKBTitleCode)TC0000831563(PQKBWorkID)10880837(PQKB)10338165(MiAaPQ)EBC1129724(Au-PeEL)EBL1129724(CaPaEBR)ebr10662564(CaONFJC)MIL455390(OCoLC)829141034(EXLCZ)99256000000009853420121005d2013 uy 0engur|n|---|||||txtccrHuman blood groups /Geoff Daniels ; foreword by Ruth Sanger3rd ed.Chichester, West Sussex John Wiley & Sons20131 online resource (544 p.)Bibliographic Level Mode of Issuance: Monograph1-4443-3324-0 Includes bibliographical references and index.Cover -- Title page -- Copyright page -- Contents -- Foreword to 1st edition -- Preface to the third edition -- Some abbreviations used -- 1: Human Blood Groups: Introduction -- 1.1 Introduction -- 1.2 Blood group terminology -- 1.2.1 An internationally agreed nomenclature -- 1.2.2 Antigen, phenotype, gene and genotype symbols -- 1.2.3 Blood group systems -- 1.2.4 Collections -- 1.2.5 Low frequency antigens, the 700 series -- 1.2.6 High frequency antigens, the 901 series -- 1.2.7 Blood group terminology used in this book -- 1.3 Chromosomal location of blood group genes -- 1.4 DNA analysis for blood group testing -- 1.4.1 Clinical applications of molecular blood grouping -- 1.4.2 Current and future technologies -- 1.5 Structures and functions of blood group antigens -- 1.5.1 Membrane transporters -- 1.5.2 Receptors and adhesion molecules -- 1.5.3 Complement regulatory glycoproteins -- 1.5.4 Enzymes -- 1.5.5 Structural components -- 1.5.6 Components of the glycocalyx -- 1.5.7 What is the biological significance of blood group polymorphism? -- References -- 2: ABO, H, and Lewis Systems -- Part 1: History and introduction -- Part 2: Biochemistry, inheritance, and biosynthesis of the ABH and Lewis antigens -- 2.2 Structure of ABH, Lewis, and related antigens -- 2.2.1 Glycoconjugates expressing ABH and Lewis antigens -- 2.2.2 Carbohydrate determinants -- 2.3 Biosynthesis, inheritance, and molecular genetics -- 2.3.1 H antigen -- 2.3.2 ABO antigens -- 2.3.3 Lewis antigens -- 2.3.4 Lex, Ley, and sialyl-Lex -- 2.3.5 Other fucosyltransferase genes -- Part 3: ABO, H, and secretor -- 2.4 A1 and A2 -- 2.4.1 A1- and A2-transferases (GTA1 and GTA2) and the genes that produce them -- 2.4.2 A1 and A2 determinants differ quantitatively and qualitatively -- 2.4.3 Aint -- 2.5 ABO phenotype and gene frequencies -- 2.6 Secretion of ABO and H antigens.2.6.1 Frequencies -- 2.6.2 Quantitative aspects -- 2.6.3 Sew -- 2.6.4 A, B, and H in plasma -- 2.7 Subgroups of A -- 2.7.1 A3 -- 2.7.2 Aend (Afinn, Abantu) -- 2.7.3 Ax -- 2.7.4 Am -- 2.7.5 Ay -- 2.7.6 Ael -- 2.7.7 Aw -- 2.7.8 Do non-deletional O alleles produce any A antigen? -- 2.8 Subgroups of B -- 2.8.1 B3 -- 2.8.2 Bx -- 2.8.3 Bm -- 2.8.4 Bel -- 2.8.5 Other subgroups of B -- 2.9 Amos and Bmos -- 2.10 A and B gene interaction -- 2.10.1 Allelic competition -- 2.10.2 Allelic enhancement -- 2.11 Overlapping specificities of A- and B-transferases (GTA and GTB) -- 2.11.1 B(A) and A(B) -- 2.11.2 cisAB -- 2.12 H-deficient phenotypes -- 2.12.1 Genetics of red cell H-deficient phenotypes -- 2.12.2 Red cell H-deficient, non-secretor -- the Bombay phenotype -- 2.12.3 Red cell H-partially deficient, non-secretor -- 2.12.4 Red cell H-deficient, secretor -- 2.12.5 Other H-deficient phenotypes -- 2.12.6 I and i expression in H-deficient phenotypes -- 2.13 Acquired alterations of A, B, and H antigens on red cells -- 2.13.1 Acquired B -- 2.13.2 Alterations in leukaemia patients -- 2.13.3 Other acquired changes in ABO antigens -- 2.13.4 In vitro enzymatic degradation of A, B, and H antigens -- 2.13.5 Modification of antigen expression by polyethylene glycol (PEG) -- 2.14 ABH antibodies and lectins -- 2.14.1 Anti-A and -B -- 2.14.2 Anti-A,B of group O serum -- 2.14.3 Clinical significance of ABO antibodies -- 2.14.4 ABO autoantibodies -- 2.14.5 ABO and transplantation -- 2.14.6 Monoclonal antibodies -- 2.14.7 Anti-H -- 2.14.8 Anti-HI and -Hi -- 2.14.9 Lectins -- Part 4: Lewis system -- 2.15 Lea and Leb antigens and phenotypes -- 2.15.1 Red cells -- 2.15.2 Secretions -- 2.15.3 Plasma -- 2.15.4 Uptake of Lewis antigens by red cells -- 2.15.5 Development of Lewis antigens -- 2.15.6 Lewis antigens during pregnancy -- 2.16 Antigen, phenotype, and gene frequencies.2.16.1 Red cells -- 2.16.2 Secretions -- 2.17 Lewis antibodies -- 2.17.1 Anti-Lea -- 2.17.2 Anti-Leb -- 2.17.3 Anti-ALeb -- 2.17.4 Clinical significance of Lewis antibodies -- 2.17.5 Lewis antibodies and renal transplantation -- 2.18 Other antigens associated with Lewis -- 2.18.1 Leabx, the antigen originally called Lex -- 2.18.2 Lec and Led -- 2.18.3 Lex, Ley, and sialyl-Lex -- Part 5: Tissue distribution, disease associations, and functional aspects -- 2.19 Expression of ABH and Lewis antigens on other blood cells and in other tissues -- 2.19.1 Leucocytes -- 2.19.2 Platelets -- 2.19.3 Other tissues -- 2.19.4 Tumours -- 2.20 Associations with disease -- 2.20.1 Bacterial infections -- 2.20.2 Viral infections -- 2.20.3 Malaria -- 2.20.4 Clotting -- 2.20.5 Pancreatic cancer -- 2.20.6 Fucosidosis -- 2.21 Functional aspects -- References -- 3: MNS Blood Group System -- 3.1 History and introduction -- 3.2 Biochemistry and molecular genetics -- 3.2.1 Glycophorins -- 3.2.2 Glycophorin A (CD235A) -- 3.2.3 Glycophorin B (CD235B) -- 3.2.4 Cloning and organisation of the genes for GPA, GPB, and GPE -- 3.3 MN and Ss polymorphisms -- 3.3.1 M and N antigens (MNS1 and MNS2) -- 3.3.2 S and s antigens (MNS3 and MNS4) -- 3.3.3 Antigen, gene, and phenotype frequencies -- 3.3.4 Inheritance -- 3.4 Effects of enzyme treatment on the MNSs antigens -- 3.4.1 Proteases -- 3.4.2 Sialidase -- 3.5 The rare glycophorin A-deficient phenotypes En(a−) and MK -- 3.5.1 En(a−) -- 3.5.2 MK -- 3.5.3 Anti-Ena, anti-Wrb, and the determinants they define -- 3.5.4 Pr and Sa antigens and antibodies -- 3.6 U antigen and the GPB-deficient phenotypes S- s- U− and S- s- U+var -- 3.6.1 U (MNS5) and anti-U -- 3.6.2 Biochemistry -- 3.6.3 Molecular genetics -- 3.6.4 Frequency studies -- 3.7 M and N variants representing amino acid substitutions within the N-terminal region of GPA and GPB.3.7.1 Mg (MNS11) -- 3.7.2 Mc (MNS8) -- 3.7.3 Fine specificity of MN antibodies -- 3.7.4 He (MNS6) and Me (MNS13) -- 3.8 The Miltenberger series -- 3.9 Hybrid glycophorins and the low frequency antigens associated with them -- 3.10 GP(A-B) variants -- 3.10.1 GP.Hil (Mi.V) and the Hil (MNS20) antigen -- 3.10.2 GP(A-B) hybrids associated with S antigen -- 3.10.3 SAT (MNS36) -- 3.10.4 En(UK) -- 3.11 GP(B-A-B) variants -- 3.11.1 GP.Mur (Mi.III), GP.Hop (Mi.IV), GP.Bun (Mi.VI), and GP.HF (Mi.X) -- 3.11.2 He (MNS6) -- 3.12 GP(A-B-A) variants -- 3.12.1 GP.Dane (Mi.IX) -- DANE (MNS32) and ENDA (MNS44) -- 3.12.2 GP.Vw and GP.Hut -- Vw (MNS9), ENEH (MNS40), and Hut (MNS19) -- 3.12.3 GP.Nob (Mi.VII) and GP.Joh (Mi.VIII) -- Hop (MNS26), Nob (MNS27), and ENKT (MNS29) -- 3.12.4 GP(A-B-A).KI -- 3.12.5 GP(A-B-A).Sat -- 3.13 Further details on Hil, TSEN, MINY, Mur, and Mia -- antigens associated with hybrid glycophorins -- 3.13.1 Hil (MNS20), TSEN (MNS33), and MINY (MNS34) -- 3.13.2 Mur (MNS10) -- 3.13.3 Mia (MNS7) -- 3.14 GP(B-A)-associated variants -- 3.14.1 Dantu (MNS25) -- 3.14.2 Sta (Stones, MNS15) and ERIK (MNS37) -- 3.15 Antigens associated with GPA amino acid substitutions proximal to the membrane and with abnormal expression of Wrb -- 3.15.1 HAG (MNS41) and ENEP (MNS39) -- 3.15.2 MARS (MNS43) and ENAV (MNS42) -- 3.15.3 ENEV (MNS45) -- 3.16 Other low frequency antigens of the MNS system -- 3.16.1 Vr (MNS12) -- 3.16.2 Mta (Martin, MNS14) -- 3.16.3 Ria (Ridley, MNS16) -- 3.16.4 Cla (Caldwell, MNS17) -- 3.16.5 Nya (Nyberg, MNS18) -- 3.16.6 Mv (MNS21) -- 3.16.7 Far (MNS22) -- 3.16.8 sD (Dreyer, MNS23) -- 3.16.9 Mit (Mitchell, MNS24) -- 3.16.10 Or (Orriss, MNS31) -- 3.16.11 Osa (MNS38) -- 3.16.12 MNTD (MNS46) -- 3.17 Antigens associated with atypical glycophorin glycosylation -- 3.17.1 Hu, M1, Tm, Sj, and Can -- 3.17.2 T, Tn, and Cad.3.18 M, N, S, s, and U antibodies -- 3.18.1 Human anti-M -- 3.18.2 Human anti-N -- 3.18.3 Clinical significance of anti-M and -N -- 3.18.4 Anti-N and renal dialysis -- 3.18.5 Glucose-dependent antibodies -- 3.18.6 Monoclonal and recombinant anti-M and -N -- 3.18.7 Lectins -- 3.18.8 Anti-S -- 3.18.9 Anti-s -- 3.18.10 Anti-U -- 3.18.11 Anti-UZ and -UX -- 3.19 GYPA mutation assay -- 3.20 Association with Rh -- 3.21 Glycophorins as receptors for pathogens -- 3.21.1 Glycophorins and malaria -- 3.21.2 Other pathogens -- 3.22 Development and distribution of MNS antigens -- 3.23 Function and evolution of glycophorins -- References -- 4: P1PK, Globoside, and FORS Blood Group Systems, plus Some Other Related Blood Groups -- 4.1 Introduction -- 4.2 Biochemistry, biosynthesis, and genetics -- 4.3 P1 (P1PK1) and anti-P1 -- 4.3.1 Frequency and inheritance -- 4.3.2 Variation in strength -- 4.3.3 Development and distribution -- 4.3.4 Other sources of P1 substance -- 4.3.5 Biochemistry and biosynthesis -- 4.3.6 Anti-P1 -- 4.4 Pk phenotype, Pk (P1PK3) antigen, and anti-Pk -- 4.4.1 Pk phenotype -- 4.4.2 Pk antigen, biochemistry, and biosynthesis -- 4.4.3 Pk on other cells -- 4.4.4 Anti-Pk -- 4.5 NOR (PIPK4) antigen and polyagglutination -- 4.6 P (GLOB1) antigen and anti-P -- 4.6.1 P antigen -- 4.6.2 Biochemistry and biosynthesis -- 4.6.3 Anti-P -- 4.7 FORS1 and the Forssman glycolipid -- 4.8 LKE and anti-LKE -- 4.8.1 Frequency and inheritance of LKE -- 4.8.2 Biochemistry and biosynthesis -- 4.8.3 Variation in strength of LKE -- 4.8.4 Development and distribution -- 4.8.5 Involvement of other P antigens -- 4.8.6 Anti-LKE -- 4.9 Sialosylparagloboside and PX2 antigen -- 4.10 p Phenotype and anti-PP1Pk -- 4.10.1 Frequency and inheritance of p phenotype -- 4.10.2 Molecular genetics of p phenotype -- 4.10.3 Biochemical effects of p phenotype.4.10.4 Antibodies in serum of p individuals.Blood groupsBlood groups.612.1/1825Daniels Geoff870782MiAaPQMiAaPQMiAaPQBOOK9910813685003321Human blood groups2126758UNINA