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.

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 .

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 study the gene expression profiles of megakaryocytes(MKs) from human cord blood CD34+ cells in vitro expanded and to understand megakaryopoiesis at the molecular level. Methods CD34+ cells were isolated using density gradient centrifugation and magnetic activated cell sorting. The cells were cultured and stimulated with recombinant human TPO ( 100 ng/ml). After 12 days, the MKs fraction was separated using an anti-CD41 monoclonal antibody by immunomagnetic sorting. The gene expression profiles of MKs, non-MKs as well as meg-01 cells were studied by gene chip assay. THBSI, HOX A9,β-actin, lL-8,Annexin A6, FGF-8 were selected to validate the gene chip results by RT-PCR. Results A total of 116 genes between MKs and non-MKs cells were significantly different, 52 genes were up-regulated and 64 genes were down-regulated. In addition, 158 genes between MKs and meg-01 cells were significantly different, 71 genes were up-regulated and 87 genes were down-regulated. THBSI showed higher expression in MKs than in non-MKs. HOXA9 showed lower expression in MKs than in non-MKs. The expression of β-actin did not show any significant difference in MKs and non-MKs. IL-8 showed higher expression in MKs than in meg-01 cells, while ANXA6 showed lower expression in MKs than in meg-01 cells. The expression of FGF-8 did not show any significant difference between MKs and meg-01 cells. Conclusions MKs, non-MKs and meg-01 cells show different gene expression profiles. The regulatory genes include stress response genes,immune related genes, DNA synthesis and repair genes, metabolism genes, pro-onco genes and tumor suppressor genes.

0.05),but the numbers of CD41+ cells and platelets were increased significantly(P

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.