Objective To identify para-Bombay phenotype AB h m. Method ABO and H phenotype were typed. Absorption and elution were performed. Saliva was tested by inhibitory reaction. Direct sequencing was performed and family study was done. Results Proband was typed as rare para-Bombay phenotype AB h mand anti-H was detected in his serum. Family study suggested that the inheritance was autosomal recessive. Conclusion Rare AB h m phenotype was identified and anti-H has been detected in his serum.

Osteoarthritis ( OA) is a chronic joint disease characterized by degeneration of articular cartilage and changes of subchondral bone play an important role in the occurrence and development of OA .Recent studies have found that change in the struc-ture and mechanical properties of subchondral bone is one of the main pathological processes in OA .To confirm the role of subchondral bone in OA process can provide not only more details about the pathogenesis of OA , but also new targets for treatment .Early diagnosis and treatment of OA may be possible by detecting radiographic and genomics of subchondral bone .We review subchondral bone chan-ges andits role in OA process in aspects of biomechanics , biology, radiological and genomics .

Objective To investigate the molecular basis for Jk(a b ) phenotype.Methods Routine serologic testing for phenotype.Genomic DNA covering 4～11 exons and partial introns of JK gene was amplified by ploymerase chain reaction.The PCR products were excised and purified from agarose gels with a kit,then fragments were directly sequenced.Results G mutated to A in the 3'acceptor splice site of intron 5;A to G at 78 site from the 3'end of intron 3;C to T at 84 site from the 5'end of intron 8; A to G at 588 site of exons ( exon 7); G to A at 838 site of exons (exon 9).The splice site mutation (G→A) of intron 5 may cause the skipping of exon 6.Conclusion G to A mutation in the 3'acceptor splice site of intron 5 maybe one of the molecular basis for Jk(a-b-) phenotype

Objective To identify the p phenotype. Method P blood group system was identified using p phenotype cells,anti PP 1 P k antiserum,and direct DNA sequencing.Result and Conclusion Proband was typed as p, with rare anti PP 1 P k in the serum,family study suggested that inheritance was autosomal recessive.

0.05). The absolute counts of RhD(+) cell of 2 patients at 3 different times were 0.124?10 12 /L, 0.245 ?10 12 /L and 0.517?10 12 /L respectively.Conclusion FCM can be used to detect RhD antigen and perform RhD(+) cell counts in patients with RhD(-) who received incompatible blood.

AIM:To study the effects of lipopolysaccharide(LPS), interleukin-6(IL-6)and tumor necrosis factor ? (TNF?) on tissue factor(TF) expression of astrocytes. METHODS:Astrocytes were identified with anti-glial fibrillary acidic protein antibody. The TF activity of cell lysate was measured with one stage clotting assay. RESULTS:TF activity of astrocytes of LPS,IL-6,TNF? groups were obviously higher than that of the control group( P

Objective : To investigate the prevalence of hepatitis B virus ( HBV ) infection among volunteer blood donors in Hangzhou City, and to evaluate the residual risk of transfusion-transmitted HBV infections. Methods : Data pertaining to volunteer blood donors in Hangzhou City from 2016 to 2019 were retrieved from the blood donor management system. Hepatitis B surface antigen ( HBsAg ) was detected by enzyme-linked immunosorbent assay ( ELISA ) and HBV DNA was detected using nucleic acid testing. The incidence/window period model was employed to assess the residual risk of HBV transmitted through transfusion from donors. Results : The prevalence of HBV infections was 0.56% among the 320 755 first-time donors and 0.13% among the 279 816 repeat donors in Hangzhou City from 2016 to 2019, and a higher prevalence of HBV infection was detected among first-time donors than among repeat donors ( P<0.05 ). The residual risks of transfusion-transmitted HBV infection were 296.38 per million person-times ( 95%CI: 277.57 to 315.19 per million person-times ) and 98.79 per million person-times ( 95%CI: 87.15 to 110.43 per million person-times ) among first-time and repeat donors with positive HBsAg, and were 86.79 per million person-times ( 95%CI: 76.60 to 96.98 per million person-times ) and 28.93 per million person-times ( 95%CI: 22.63 to 35.23 per million person-times ) among first-time and repeat donors tested positive for HBV DNA, respectively. Conclusions There is still a residual risk of HBV infection transmitted through transfusion from blood donors in Hangzhou City. Nucleic acid testing may remarkably reduce the residual risk of transfusion-transmitted HBV infection in blood donors.

Objective To detect fetal RhCcEe genotype from fetal DNA in maternal plasma for noninvasive prenatal diagnosis.Methods DNA from maternal plasma sample was extracted by use of QIAamp DNA Kit. The existence of fetal DNA was confirmed by amplified fetal SRY gene. The fetal RhCcEe gene was amplified by polymerase chain reaction (PCR) from 30 pregnant maternal plasma. The results of fetal RhCcEe genotype were evaluated retrospectively by the serologic analysis of infant and pregnant woman RhCcEe phenotype.Results Among the 30 samples, 13 were the same phenotypes between mother and infant, 17 were different. When mother phenotypes were RhCC, cc, EE and ee homozygous, the deleted allele gene can be successfully amplified from mother plasma.Conclusion Noninvasive fetal RhCcEe genotyping is reliable. When the mother was homogyzous, genotyping the fetal CcEe alleles was very significant and useful for HDN (hemolysis disease of newborn) diagnosis and therapy.

Objective To establish a PCR sequencing-based typing (PCR-SBT) method for simultaneous genotyping of human platelet antigen HPA-1 to HPA-16w.Methods All DNA polymorphism sites of HPA-1 to HPA-16w were obtained from the immuno polymorphism database.The specific primers were designed using Primer Premier 5.0 software to amplify nucleotide acid fragments encompassing each HPA polymorphism site.The primer sequence and PCR condition were optimized to obtain specific and single amplification product.The PCR product was purified and then sequenced to determine the HPA genotypes.Two standard DNA samples were detected using the HPA PCR-SBT method to examine the accuracy d this method.Sixteen reference samples (including 6 interference samples with HPA gene mutations) provided by 14th platelet immunology workshop of international society of blood transfusion (ISBT) in 2008 were also tested by this home-brew HPA PCR-SBT method.Results Total eleven pairs of primers were designed to amplify and sequence the sixteen HPA systems.The HPA genotypes of two standard samples were 1aa/2aa/3ab/4aa/5ab/6aa/7aa/8aa/9aa/10aa/11aa/12aa/13aa/14aa/15aa/16aa and 1aa/ 2aa/3aa/4aa/5aa/6aa/7aa/8aa/9aa/10aa/11aa/12aa/13aa/14aa/15aa/16aa,respectively.The 256 HPA genotypes of 16 reference samples were clear.128 genotypes among them were completely accordance with the results provided by ISBT report.Conclusions The PCR-SBT assay combining high-throughput DNA sequencer established in the study provides a simple,rapid and accurate method for HPA-1 to HPA-16w systems genotyping.The assay is suitable for routine clinical HPA genotyping and shows a broad prospect in further applications.

Objective To investigate the effects of methylated CpG islands in the promoter region on the expression of killer cell immunoglobulin-like receptor 3DL1 (KIR3DL1).Methods Three voluntary unpaid blood donors carrying high expression allele KIR 3DL1*01502 and three donors carrying low expres-sion allele KIR3DL1*005 were recruited in this study .The nucleotide sequences and the methylated CpG islands in the promoter regions of KIR 3DL1*01502 allele and KIR3DL1*005 allele were analyzed .The NK cells expressing KIR3DL1*01502 and KIR3DL1*005 were respectively treated with 5-aza for the dem-ethylation of CpG islands within the promoters .The expression of KIR3DL1 protein on the surface of NK cells was measured with flow cytometer .Results Two differences at nucleotide sites -65 and -269 were detected within the promoter regions of KIR3DL1*01502 and KIR3DL1*005, resulting in two distinct CpG islands.The CpG islands within the promoter of KIR 3DL1*01502 allele were highly methylated .The ex-pression of KIR3DL1 protein on NK cells which carried KIR 3DL1*01502 allele was significantly increased after the demethylation of CpG islands .However , the treatment of demethylation had no significant effects on the expression KIR3DL1 protein on NK cells harboring KIR3DL1*005 allele.Conclusion The methylated CpG islands within the promoter of KIR 3DL1*01502 allele affected the antigen expression on the surface of NK cells.Different KIR3DL1 alleles might show different mechanisms in regulating antigen expression .