A transfusion-transmitted hepatitis E case by blood from a donor infected via the zoonotic food-borne route and the progress of HEV markers in the entire course are demonstrated. Further studies are needed to clarify the epidemiology and the transfusion-related risks for HEV even in industrialized countries.

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Summary. Cytomegalovirus (CMV) infection in 28 adult patients after cord blood transplantation (CBT) from unrelated donors was compared with that after bone marrow transplantation from HLA (human leucocyte antigen)-matched related (R-BMT) and unrelated (U-BMT) donors. Positive CMV antigenaemia was seen in 19 (79%) of 24 CMV-seropositive patients at a median of 42 d (range 29-85 d) after CBT, but in zero of four CMV-seronegative patients. This did not differ significantly from values observed after R-BMT and U-BMT (66%, P ¼ 0AE22, and 60%, P ¼ 0AE15 respectively). Based on the antigenaemia results, 16 patients (67%) received pre-emptive ganciclovir therapy from a median of 47 d (range 36-67 d) after CBT. This proportion was higher than that observed after R-BMT (28%, P ¼ 0AE0048), but did not differ from that after U-BMT (50%, P ¼ 0AE21). In addition, the probability of requiring more than two courses of ganciclovir therapy after CBT (21%) was higher than after R-BMT and U-BMT (0%, P ¼ 0AE015 and 0AE039 respectively). One patient (5%) developed CMV disease after U-BMT, whereas no patients developed CMV disease after CBT or R-BMT. The CMV serostatus, use of a steroid and HLA disparity affected the probability of requiring ganciclovir therapy after CBT (P ¼ 0AE024, 0AE032 and 0AE017 respectively). These results suggest that recovery of CMV-specific immunity after CBT is delayed when compared with BMT.

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Heat-shock proteins (HSPs) act as molecular chaperones binding endogenous antigenic peptides and transporting them to major histocompatibility complexes. HSPs chaperone a broad repertoire of endogenous peptides including tumor antigens. For the immunotherapy of tumors, a strategy using HSPs may be more advantageous than other procedures because the identification of each tumorspecific antigen is not necessary. In this study, the efficacy of immunotherapy against minimal residual leukemia cells using HSP preparations was evaluated.HSP70 and GP96 were purified from syngeneic leukemia cell line A20 and immunized into BALB/c mice during the reconstitution period of the immune system after syngeneic bone marrow transplantation. In this procedure, all mice not immunized were dead within 60 days of A20 inoculation, whereas the survival times of HSP-immunized mice were significantly prolonged. In addition, the depletion of either CD4 ؉ or CD8 ؉ T lymphocyte significantly abrogated this efficacy, indicating that both CD4 ؉ and CD8 ؉ T lymphocytes were required for tumor cell rejection.

Non-transferrin bound iron (NTBI) in serum is cleared rapidly by hepatocytes, although the mechanisms of NTBI uptake by hepatocytes are poorly understood. Dietary iron is transported into intestinal enterocytes by divalent metal transporter 1 (DMT1), which also transports iron from transferrin receptor 1 (TfR1)-mediated recycling endosome to intracytoplasm. We made an antiserum against human DMT1 protein derived from mRNA with the iron responsive element (IRE). The DMT1 detected by the antiserum was mainly observed in the membranes of duodenal enterocytes and enterocyte carcinoma (Caco2) cells, whereas DMT1 in normal liver and hepatoma (HLF) cells, was preferentially located in cytoplasm but weakly on cell surface. In addition, iron-depleted HLF increased membrane expression of DMT1, suggesting that the intracellular iron concentration regulated the DMT1 expression in hepatocytes via the iron regulatory protein (IRP)/IRE system. DMT1 overexpressing HLF by DMT1 cDNA transfection expressed DMT1 in both cytoplasm and cell membrane. Although these cells did not change TfR-dependent iron uptake, they took up a significant amount of ferrous iron. These results indicate that the DMT1 plays an important role in transporting NTBI into cells.

Summary. In the present study, we demonstrated that a close relationship exists between hepatitis C virus (HCV) infection of peripheral blood mononuclear cells (PBMCs) and cell-surface Fas expression in patients with hepatitis C, and showed the possibility of PBMCs apoptosis via a Fasmediated system. The expression of Fas on PBMCs was found by flowcytometric analysis to be significantly increased in these patients. In addition, the treatment of patients' PBMCs with anti-Fas antibody induced cell death, with nuclear condensation and fragmentation and cellular DNA fragmentation. These data indicate that the patients' PBMCs expressed a large amount of functional Fas on the cell surface and were susceptible to stimulation against Fas, causing apoptotic cell death. We then quantified the serumsoluble Fas ligand (sFasL), which was known to bind to Fas and induce the apoptotic signals into the sensitized cells.The patients' serum sFasL levels were significantly higher than those of normal subjects and showed a good negative correlation with their PBMC number. To demonstrate the correlation between Fas expression and HCV infection, nested reverse transcriptase polymerase chain reaction (RT-PCR) was performed to detect HCV RNA. Interestingly, HCV RNA was preferentially detected from Fas-positive cells but not from Fas-negative cells, which had been isolated from PBMCs by magnetic beads. These results suggest that HCV infection of PBMCs might induce Fas expression and additional stimulation such as sFasL might induce apoptosis in these Fas-expressing cells. These mechanisms, in addition to hypersplenism, may explain the decrease in the number of PBMCs observed in patients with chronic hepatitis C.

Summary. We performed a clinical comparison of unrelated cord blood transplantation (UCBT) and unrelated bone marrow transplantation in adult acute leukaemia patients in complete remission (CR) who received the same conditioning regimen, graft-versus-host disease (GvHD) prophylaxis and supportive treatment. The incidence of acute GvHD was almost the same between the two groups, but the haematopoietic recovery was delayed and the incidence of chronic GvHD was higher in the UCBT group. The probability of 2 year disease-free survival was similar between the two groups. These results suggest that adult acute leukaemia patients in CR without a suitable donor should be considered as candidates for UCBT.