This report is to outline the clinical effects of 2-ethyl-3 (4' hydroxybenzole) benzofurane (Fragivix), flavone derivative, on subiects with fragile capillaries as for capillary resistance as well as permeability.
Materials and Methods: Out of hypertensives and diabetics, 23 cases with capillary resistance below 130 mmHg according to Borbély's method were selected. Landis' method was employed for the permeability. The subjects received 600 mg Fragivix a day for a week or two.
Results: Those who showed increase in the capillary resistance more than 30 mmHg by Borbély's method were considered to be effective. Eighteen (78%) among 23 cases were found to be improved in the capillary resistance; bleeding clotting time were unchanged. The inhibition of permeability caused the decrease of water to 90% and protein to 80%, when compared with the results before the administration. Further, side effects were not seen.
The acceleration of peripheral vascular permeability and the decrease of capillary resistance at the same time have been recognized in various constitutional diseases. The author thinks it necessary to normalize the capillary resistance in terms of the prevention of hypertensive cerebral hemorrhage or vascular reinforcement and that of diabetic vascular disease and its improvement. Therefore, Fragivix seems to be of value when used to hypertensive or diabetic patients with fragile capillaries.

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Leukocytes were isolated from the peripheral blood of patients with leukemia and other blood diseases by means of differential separation using 0.83% NH₄CI solution. The lactic dehydrogenase (LDH) activity and its isozymes were measured on the supernatant fraction of thus collected leukocyte homogenate.
Leukocytes isolated from healthy men were reserved as control, in which more than 90% of collected leukocjtes composed of mature granulocytes with free of red cell.
The results are as follows.
1. The mean LDH activity of granulocytes from normal men was 320 units per 10⁶ cells with the standard deviation of 140 units. The activity was around the lower border of the normal levels in leukemias, while it was slightly higher than control in leukocyte from chronic granulocytic leukemia.
2. Agar-gel electrophoresis disclosed five different isozymes on normal human granulocyte, while were named as LDH_5,4,3,2 and LDH₁ in the order from the cathode. The activities of these fractions were found to be in due of this order with the highest peak in LDH₅.
3. The LDH isozyme pattern of acute leukemic cells were characterized by a extreme increase in LDH³, while turned into the highest peak among the five fractions, with concomitant decrease in LDH₅. A similar but less trend of LDH isozyme pattern was demonstrated in leukocytes from chronic granulocytic leukemia.
4. Singular and characteristic LDH isozyme patterns were observed on leukocytes from patients with various blood diseases such as aplastic anemia, malignant lymphoma, myeloma and megaloblastic anemia,
5. Significance of the characteristic isozyme patterns of leukemic cells was discussed mainly from the view point of its metabolism and turnover. It was assumed that such changes were of tumor specific alterations.

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The purpose of this paper was to study of the regulation of mechanism of erythropoiesis in polycythemia vera.
In polycythemic state (Hematocrit: 76%), plasma and urinary erythropoietin levels were virtually undetectable. On the other hand, the presence of an erythropoietin inhibitor was evidenced in the plasma from the patients with this disorder. Furthermore, polycythemia vera marrow showed no significant response to erythropoietin in vitro, while normal human marrow showed a markd increase of the incorporation of ³H-thymidine in erythroid cells when this hormone was added.
Lowering hematocrit by means of serial phlebotomies, the increase in erythropoietin excretion and reticulocytes were observed in polycythemia vera. Moreover, the increase of the in vitro incorporation of ³H-thymidine in erythroid cells was found in response to the severe anemia.
These observations indicate that two different controlling mechaisms of erythropoiesis in polycythemia vera are at work—the usual erythropoietin mechanism when the patient is at anemic levels and another more autonomous control as the red cell count reaches polycythemic values.

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A 62-year-old female with multiple myeloma was reported.
She had palpitation, shortness of breath and lumbago and then she could not walk.
Laboratory examination showed anemia, granulocytopenia, relative lymphocytosis, thrombocytopenia, and myeloma cells in the peripheral blood. The proliferation of myeloma cell was found in the bone marrow. Hyperproteinemia which showed γ-G (κ-type) by immunoelec trophoreisis and sometimes proteinuria of Bence-Jones type were found.
After 5 months of the admission, she developed sudden abdominal pain and tarry stool and died on the next day.
Autopsy revealed myelomatous proliferation in all bone system-sternum, ribs, skull, vertebrae and femurs. Metastatic myelomatous proliferation was found in the liver, spleen, kidney, adrenal gland and pancreas and markedly in esophagus, stomach and small intestine. The latent localized carcinoma of thyroid gland was also found.
Metastasis of myeloma cells to the other organs than bone system, the cause of death, especially the bleeding from gastric ulcer and the complication of carcinoma were discussed.

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A 45-year-old male was admitted because of nasal bleeding and allergic purpura.
Positive hematological laboratory studies showed slight normochromic anemia, platelets 4000, reticulocytes 19‰, positive direct and negative indirect erythrocyte Coombs' test.
After admission, allergic purpura disappeared, but anemia was aggravated, platelets 2900, bleeding time over 30 minutes, reticulocytes 69∼90‰, and other studies revealed a strongly positive erythrocyte Coombs' test and warm type incomplete antibody, showing positive reaction to anti-1gG.
Platelet cold agglutination reaction and platelet Coombs' consumption test were positive and serum immunoelectrophoresis showed decreased IgG, IgA and IgM, deficiency of hemopexin and β1CA.
Bleeding tendencies were subsided, platelet count increased to about 100,000 and reticulocyte count decreased after treatment of 40 mg prednisolone a day.
After splenectomy, platelet count was about 200,000 and antiplatelet antibody became negative, even in the maintenance of 5 mg prednisolone a day.
Erythrocyte Coombs' test turned to be negative after therapy of 6-mercaptopurine.

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A 43-year-old male was admitted because of remittent fever and generalized lymphadenopathy in March, 1966. The fever was subsided and the lymphadenopathy, histologically reactive reticulosis, diminished in size after the treatment with prednisolone and cyclophosphamide. The same symptoms recurred in August, with the abrupt development of splenomegaly, monoclonal IgM(κ), tuberculin anergy, and positive Cooms'test at the beginning of November. It was remarkable that atypical cells with perinuclear halo were present in the biopsy specimen of a lymph node and the smears of bone marrow and peripheral blood. The cells vanished from the peripheral blood during two months of the terminal stage with the disappearance of these immunologic aberrations. These atypical cells were thought to be differentiated from lympho-reticular cell series, and to be related to the presence of monoclonal IgM. After one year's clinical course, he died of gastrointestinal bleeding. It was found at autopsy that atypical lymph-reticular cells of primitive type infiltrated in the lymph nodes, bone marrow, liver and spleen, though the cells with perinuclear halo diminished markedly in number.

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A Case with β thalassemia and a case with hemolytic anemia resembling thalassemia were reported previously. Both died after severe hepatic disorder.
The former was normal in liver function test and only iron deposit in parenchymal cells remarkably found on liver biopsy specimen. Two years later, this patient was readmitted and 200 ml of blood transfusion was performed. Then, serious hepatic disorder occured and he died 2 months later. Highly degenerated hepatic parenchyma, fibrosis and iron deposit were pointed out at autopsy.
Hepatic function test of the second patient was normal in serum transaminase activity and strongly high colloidal reactions were reported at her admission. Then, hepatic disorder progressed gradually and died after 7 months. Desferrioxamine B was not effective in this case.
Hepatic disorder should be cautiously remirded in treating thalassemia which is resistant to any way of therapy or medication with exception of blood transfusion.

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A 28-year-old female was seen at Kyoto Univercity Hospital on Oct. 13, 1967, with a chief complaint of swelling of the generalized lymph nodes. A diagnosis of chronic myelocytic leukemia (CML) was made from the peripheral and bone marrow smears, a low score of leukocyte alkaline phosphatase and a positive Philadelphia chromosome (Ph¹). Biopsy of the lymph nodes revealed leukemic infiltration with immature cells of the myeloid series. (myeloblastoma) On April 1968, leukemic hiatus in the bone marrow smears, a high score of leukocyte alkaline phosphatase and Ph¹ with hyperdiploidy of the chromosome were recognized, by which a diagnosis of the blastic crisis was made. The lymph nodes grew larger in size and radiation and chemotherapy were performed without effect.
It was discussed that the marked lymph node enlargement was a poor prognostic sign appearing in the course of CML before blastic crisis.

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