The method for prolonged preservation of platelet concentrate, especially the significance of addition of PGE₁, glycyrrhizin and α-tocopherol in the preservation of platelet concentrate, was investigated and the following results have been obtained.
1. It was found that PGE₁ added to platelet concentrate presserved under liquid form produced a desirable effect on platelet membrane integrity, mitigating the morphological change of platelet and its disintegration, and that this effect was particularly remarkable during preservation at 4°C. It should be noted, however, that PGE₁ exhibited a strong inhibitory effect on platelet aggregation.
2. Glycyrrhizin was also effective in the maintenance of platelet integrity, its inhibitory effect on platelet disintegration being particularly marked during preservation at 4°C. Further, glycyrrhizin mitigated the reduction in platelet aggregation, no matter whether platelet concentrate was preserved at 4°C or room temperature. These findings suggest that glycyrrhizin is also effective in the maintenance of functional platelet membrane integrity.
3. α-Tocopherol was effective in the maintenance of the integrity of platelet membrane, be it preserved at 4°C or room temperature; in either case it mitigated the morphological change of platelet and its disintegration. It should be noted, however, that α-tocopherol had a tendency to inhibit platelet aggregation, especially during preservation at 4°C.
It may therefore be concluded that PGE₁, glycyrrnizin and α-tocopherol are effective in the prolonged preservetion of PC.

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Surgical hemorrhage (1413±1245ml), which was caused during radical operation of uterine cancer in 9 paitents, was treated with perioperative autologous donation (1200ml) supported by concomittant infusion of dextran solution and intraoperative blood salvage using Hemonetics Cell Saver^®.
By the intraoperative blood salvage, 255±134ml of suspension of washed red cells was obtained.
Approximately 400ml of the autodonated blood was infused to maintain the circulating blood volume until the surgical blood loss reached to 800ml.
In the meantime, the bled blood in operation field was salvaged and filtered by Bentley Reservoir Q-220F^®. The red cells were washed and concentrated to 42.1±17.4% of Hematocrit by Cell Saver. And then infused through a transfusion set mounted Paul's microfilter.
After completion of the transfusion, the circulating red cell mass remained in 71.1% of the initial value and the platelet count in 75.8%. The free hemoglobin in serum decreased from 31.5mg/dl to 22.9 after the transfusion and remained in the similar level for the subsequent seven days.
No bacterial contamination was detected in the washed and packed red cells.

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In 1979, anti-C9 antibody was found in a patient with hereditary C9 deficiency. This patient had received multiple transfusions with several units of blood. The detection of C9 deficient patients and follow-up of those transfused were done in 52, 000 patients treated at Kyushu University Hospital to investigate the frequency of C9 deficiency, and the incidence of anti-C9 precipitating antibodies in transfused patients. Transfusion reactions in recipients having anti-C9 antibody were also monitored. The study identified twelve patients with C9 deficiency (a prevalence of 0.023%). Three out of twelve patients had received transfusions. One of the patients who had received several units of blood within a week, produced low-titer anti-C9 precipitating antibody. This patient was transfused in the presence of anti-C9 precipitating antibody without evidencing transfusion reactions. No precipitating antibody was detected in the remaining two patients who had received several units of blood during the course of a single day.
These observations suggest that one of the factors that may be conducive to the development of anti-C9 antibody is the frequency of multiple transfusions. Furthermore the likelihood of transfused C9 deficient patients developing transfusion reactions is minimal.

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The results of 68 leukocyte cross-matching procedure have been assessed in order to select compatible donors for 19 febrile granulocytopenic patients with acute leukemia.
It was revealed that there was positive relationship between precounts of patients' own leukocytes and granulocyte recovery rates. This phenomenon suggested that leukocytes of marginal pool were markedly depleted and most part of transfused granulocytes might marginate along the vessel walls in leukopenic patients.
This study confirms the clinical value of lymphocytotoxicity test (LCT) in predicting the post-transfusion recovery rate of single donor granulocytes. There was a good agreement between the LCT croos-match and granulocyte recovery. In general, compatibility in the granulocytotoxicity (GCT) has not any significant value in granulocyte recovery rates.

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Polyagglutination of erythrocytes is observed when most normal ABO-compatible human serum agglutinate the tested red cells.
Recently we had a case of polyagglutination caused by the Tn antigen. Tn-polyagglutination was detected in the blood of a 78-years-old female patient with pancytopenia. The true blood group of the patient was O, but her cells had an aquired A-like specificity. Confirmation that the polyagglutination was caused by Tn activation was established by the reaction of lectins, weak aggregation with polybrene, and low sialic acid levels of red cell. This change of red cell membrane was thought to be due to somatic mutation at stem cell level.

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