Mapping the Xga red blood cell antigen in human-Chinese hamster cell hybrids

1975 ◽  
Vol 14 (3-6) ◽  
pp. 293-295 ◽  
Author(s):  
M. Fellous ◽  
P.L. Pearson ◽  
A.G.J.M. van der Linden ◽  
Meera Khan ◽  
A. Hagemeijer
1979 ◽  
Vol 24 (3) ◽  
pp. 129-137 ◽  
Author(s):  
I. Raskó ◽  
S.L. Péter ◽  
K. Burg ◽  
L. Dallmann ◽  
G. Bajszár

1981 ◽  
Vol 1 (4) ◽  
pp. 336-346
Author(s):  
C E Campbell ◽  
R G Worton

Somatic cell hybrids heterozygous at the emetine resistance locus (emtr/emt+) or the chromate resistance locus (chrr/chr+) are known to segregate the recessive drug resistance phenotype at high frequency. We have examined mechanisms of segregation in Chinese hamster cell hybrids heterozygous at these two loci, both of which map to the long arm of Chinese hamster chromosome 2. To follow the fate of chromosomal arms through the segregation process, our hybrids were also heterozygous at the mtx (methotrexate resistance) locus on the short arm of chromosome 2 and carried cytogenetically marked chromosomes with either a short-arm deletion (2p-) or a long-arm addition (2q+). Karyotype and phenotype analysis of emetine- or chromate-resistant segregants from such hybrids allowed us to distinguish four potential segregation mechanisms: (i) loss of the emt+- or chr+-bearing chromosome; (ii) mitotic recombination between the centromere and the emt or chr loci, giving rise to homozygous resistant segregants; (iii) inactivation of the emt+ or chr+ alleles; and (iv) loss of the emt+- or chr+-bearing chromosome with duplication of the homologous chromosome carrying the emtr or chrr allele. Of 48 independent segregants examined, only 9 (20%) arose by simple chromosome loss. Two segregants (4%) were consistent with a gene inactivation mechanism, but because of their rarity, other mechanisms such as mutation or submicroscopic deletion could not be excluded. Twenty-one segregants (44%) arose by either mitotic recombination or chromosome loss and duplication; the two mechanisms were not distinguishable in that experiment. Finally, in hybrids allowing these two mechanisms to be distinguished, 15 segregants (31%) arose by chromosome loss and duplication, and none arose by mitotic recombination.


Transfusion ◽  
2013 ◽  
Vol 54 (1) ◽  
pp. 86-97 ◽  
Author(s):  
Seema Kacker ◽  
Paul M. Ness ◽  
William J. Savage ◽  
Kevin D. Frick ◽  
R. Sue Shirey ◽  
...  

Transfusion ◽  
2019 ◽  
Vol 59 (12) ◽  
pp. 3767-3775 ◽  
Author(s):  
Xin Lin ◽  
Graciela Rubio ◽  
Jigar Patel ◽  
Sukanta Banerjee ◽  
Tom Frame ◽  
...  

2015 ◽  
Vol 05 (03) ◽  
pp. 004-008
Author(s):  
Mohammed Saleem E. K. ◽  
Soundarya Mahalingam ◽  
Shamee Shastri ◽  
Kamalakshi G. Bhat

AbstractThe development of red blood cell (RBC) isoimmunization with alloantibodies and autoantibodies complicate transfusion therapy in multiply transfused thalassemia patients. We conducted a study to analyse the frequency in our population. Clinical and antibody profile from 55 multiply transfused thalassemic patients who were receiving transfusions were collected and analyzed prospectively. A commercially available 3 cell antigen panel was used for the antibody screening procedure. If antibody screening with the 3-cell antigen panel was positive, an extended 11-cell antigen panel was used for antibody identification in LISS (Low Ionic Strength Solution). All patients received blood matched for only ABO and Rh (D) antigens. A total of 55 transfusion dependent â thalassemics were included in this study out of which 30 (54.55%) were males and 25(45.45%) females with a male to female ratio of 1.2: 1. Frequency of red cell alloimmunization in this study was found to be 1.8%. None of the patients developed red cell autoimmunization. The alloantibody identified in the the patient who developed alloimmunisation was was anti-K. In conclusion, the transfusion of matched blood is essential for chronically transfused beta thalassemia patients in order to avoid alloimmunization.


2020 ◽  
Vol 320 ◽  
pp. 128376
Author(s):  
Hongmei Wang ◽  
Shengbao Duan ◽  
Mingyuan Wang ◽  
Shuangshi Wei ◽  
Yezhou Chen ◽  
...  

Transfusion ◽  
2007 ◽  
Vol 47 (s1) ◽  
pp. 60S-63S ◽  
Author(s):  
Ghazala Hashmi

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