Apheresis on aged patients/donors with complicated backgrounds like ischemic heart disease, arrhythmia, and others.

Peripheral blood stem cells (PBSCs) are currently one of the most important stem cell sources for hematopoietic stem cell transplantation as well as cell therapy for ischemic heart disease or critical limb ischemia. Thus, it is sometimes necessary to collect autologous PBSCs from donors who have comorbidities. In terms yield, a sufficient number of PBSCs can be collected from donors with comorbidities for performing cell therapy if their age is < 60 years or up to a maximum of 70 years, although the number of PBSCs collected from older donors would probably be lower than that obtained from younger donors. On the other hand, granulocyte colony-stimulating factor (G-CSF) administration sometimes results in severe adverse events (AEs), such as ischemic heart disease and vascular thrombosis. Therefore, it is very important to perform strict medical check-ups according to the standards for donor operations in each country before apheresis. The apheresis procedure and G-CSF administration should be performed after administering the appropriate treatment. There is very less information available regarding AEs related to citrate administration during apheresis in aged donors with complicated medical histories. Medical staff should have knowledge of the electrocardiogram (ECG) QTc prolongation that occurs during apheresis owing to hypocalcemia caused by citrate administration, necessitating electrocardiographic monitoring of patients. Calcium should be administered during apheresis to prevent citrate related symptoms.

Expression of ABO blood-group genes is dependent upon an erythroid cell-specific regulatory element that is deleted in persons with the B(m) phenotype.

The ABO blood group is of great importance in blood transfusion and organ transplantation. However, the mechanisms regulating human ABO gene expression remain obscure. On the basis of DNase I-hypersensitive sites in and upstream of ABO in K562 cells, in the present study, we prepared reporter plasmid constructs including these sites. Subsequent luciferase assays indicated a novel positive regulatory element in intron 1. This element was shown to enhance ABO promoter activity in an erythroid cell-specific manner. Electrophoretic mobility-shift assays demonstrated that it bound to the tissue-restricted transcription factor GATA-1. Mutation of the GATA motifs to abrogate binding of this factor reduced the regulatory activity of the element. Therefore, GATA-1 appears to be involved in the cell-specific activity of the element. Furthermore, we found that a partial deletion in intron 1 involving the element was associated with B(m) phenotypes. Therefore, it is plausible that deletion of the erythroid cell-specific regulatory element could down-regulate transcription in the B(m) allele, leading to reduction of B-antigen expression in cells of erythroid lineage, but not in mucus-secreting cells. These results support the contention that the enhancer-like element in intron 1 of ABO has a significant function in erythroid cells.