[The Results of ABO/RhD Blood Group and Comparative Analysis Detected by Two Methods in Infants Younger than 6 Months].

OBJECTIVE: To detect the ABO / RhD blood type of infants younger than 6 months in different gestational age and month old with automatic microcolumn glass sphere and tube method, and compare the result of the two methods. METHODS: The data of 896 samples of infants younger than 6 months from January 2018 to February 2019 was collected. The two methods were used to detect ABO/RhD blood type in all samples and compare the detection rate of ABO/RhD antigen and ABO reverse typing and agglutination intensity of the two methods. RESULTS: Three hundred and eight cases of type A (34.4%), 281 cases of type B (31.4%), 210 cases of type O (23.4%), 97 cases of type AB (10.8%), and 896 positive cases of RhD blood type were detected out by two methods. There were no significant differences of ABO/RhD antigen agglutination intensity between two methods (P > 0.05). Except for type AB, the detection rate of ABO reverse typing in infants with type B was significantly higher than that with type A and type O (P < 0.05). The agglutination intensity of type A reverse cell was higher than type B reverse cell (P < 0.05). The fully automatic microcolumn glass sphere method exhibited higher detection rate of ABO reverse typing in the samples of type A and type O group and agglutination intensity of ABO reverse typing in all types as compared with the tube method (P < 0.05). The detection rate and agglutination intensity of ABO reverse typing in term group were significantly higher than those in preterm group (P < 0.05). The fully automatic microcolumn glass sphere method exhibited higher detection rate of ABO reverse typing and agglutination intensity compared with the tube method between two groups (P < 0.05). The detection rate and agglutination intensity of ABO reverse typing in group IV (4-6 months old) were significantly higher than those in groups I, II and III (young than 3 months old) (P < 0.05). The fully automatic microcolumn glass sphere method exhibited higher detection rate of ABO reverse typing in I, II, III groups and agglutination intensity of ABO reverse typing in the 4 groups compared with the tube method (P < 0.05). CONCLUSION: ABO / RhD blood group antigen can be accurated detected in majority of infants, but the detection rate of ABO antibody is related to gestational age and month age of infants. The detection rate and agglutination intensity of the fully automatic microcolumn glass sphere method in ABO reverse typing are higher than those of the tube method, especially for premature infants and children within 3 months old.

[Genotyping for Auxiliary Identification of Anti-C Alloantibody with Anti-f Autoantibody Mimicking Alloantibody].

OBJECTIVE: To identify the difficult antibody specificity of 1 PNH patient with blood transfusion history by genotyping. METHODS: RH typing of this patient was performed using gel card method, the antibody specificity was identified by panel cells, the RH-unrelated phenotype were excluded by genotyping method in difficult condition of serologic identification, furthmore different RH phenotype cells were used for adsorption-elution so as to re-examine the reactivity of antibodies in this patient's serum, and finally different RH phenotype cells were combined to exclude other unrelated antibodies. RESULTS: The RH phenotype presented as double population for C antigen, and positive agglutination for the other antigens. The results of RHD zygote, together with RHD and RHCE sequencing showed that the RHD genotype was homozygous RHD/RHD, and the c.122A＞G mutation did not found in RHCE gene, thus CW antigen was excluded; 48G lies in the 1st exon, the 5th exon showed nt676 G/C heterozygosity, the 2nd-4th, 6th-10th exons did not show mutations, however a new mutation was found in the 4th intron IVS4+29A＞C. It can be judged that the RH genotype was Dce/DcE, and its phenotype should be ccDEe. The anti-C alloantibody and rare anti-f autoantibody mimicking alloantibody in serum was determined by different RH phenotypic cell absorption-elution. Finally, cross-matched AB ccDEE blood units were selected for the patient and there was no adverse reactions of blood transfusion occurred. CONCLUSION: Genotyping can be auxiliarily applied to the identification of difficult antibodies in serum of a patient, thereby reducing the risk of blood transfusion.

[Comparison of Weak ABO Antigen and Normal ABO Antigen in Patients with Acute Leukemia].

OBJECTIVE: To compare the differences between weak ABO antigen patients and normal ABO antigen patients with acute leukemia, and to explore the clinical significance of weak ABO antigen in acute leukemia. METHODS: The ABO blood group was detected in 110 newly diagnosed acute leukemia patients(including 68 cases of AML and 42 cases of ALL) and 68 normal controls. Then the leukemia subtype, age, sex, laboratory test, risk status of leukemia patients, and DNA methylation of ABO promoter were compared between patients with weak and normal ABO antigen. RESULTS: The weak ABO antigen was found in patients with newly diagnosed acute leukemia, and was not found in ALL patients or normal group. No statistical differences were found in the distribution of ABO blood group, age, hepatosplenomegaly, lymphadenovarix, plt, precursor cell clusters derived from bone marrow, immunopheno-typing, LDH level, and risk status between AL patients of weak and normal ABO antigen groups (P>0.05). Compared with patients in normal ABO antigen group, the pateins in weak ABO antigen group had higher percentage of male(77.8% vs 30%), lower WBC(32.26×109/L vs 82.69×109/L) and Hb level(64.00 g/L vs 85.94 g/L) and higher DNA methylation level (18.91% vs 10.76%) (P<0.05). CONCLUSION: The cases of weak ABO antigen frequently appear in the male AML patients, the DNA methylation level of ABO gene promoter in patients with weak ABO antigen is significantly higher than that in patients with normal ABO antigen.

[A single E726Q mutation in the membrane proximal α-helix of integrin ß3 subunit induces membrane blebbing by disrupting the membrane-actin cortex interaction].

The membrane proximal α helix of integrin ß subunit cytoplasmic tails plays an important functional role by interacting with various intracellular proteins, namely talin, α-actinin or skelemin. This study was designed to investigate the functional role of 5 highly conserved charged amino acids (R(724), K(725), E(726), E(731), E(733)) within this α helix by site-directed mutagenesis. The result showed that CHO cells expressing the αIIbß3E726Q mutant had the most prominent phenotype and characterized by defective cell spreading on immobilized fibrinogen. In addition, this E726Q mutation induced membrane blebbing in cells adherent on fibrinogen, and this blebbing could be inhibited by the myosin light chain ATPase inhibitor blebbistatin. It is concluded that the membrane proximal α-helix of integrin ß3 subunit is important in linking the phospholipid membrane to the submembraneous actin cortex.