Serum ceruloplasmin values were determined in cases of hypoplastic anemia and acute leukemia, and their clinical significance was studied with regard to prognosis.
In hypoplastic anemia, serum ceruloplasmin was high in cases with improvement. Cases without improvement were divided into two groups: the acute form with high ceruloplasmin value and intense clinical symptoms, and with low ceruloplasmin value and scarcely any intense clinical symptoms.
Prognosis was usually poor in hypoplastic anemia with decreased platelet counts and nucleated cells in the bone marrow, while cases of high serum ceruloplasmin values and mild symptoms among these may recover.
Fluctuations of serum ceruloplasmin in cases of hypoplastic anemia with recovery following treatment were similar to those of erythropoietin.
High serum ceruloplasmin values in acute leukemia at the time of initial examination (before treatment) indicated longer period of survival. The 50% survival period was 9.6 months in the group with serum ceruloplasmin values above 40 mg/dl, while it was 2.3 months in the group with serum ceruloplasmin values less than 25 mg/dl.
Determination of serum ceruloplasmin values through the course of acute leukemia indicated a decrease towards the terminal stage in many cases.

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Erythropoiesis in human bone marrow has been studied on the basis of the erythroblast compartments classified by their cytoplasm stainabilities. Since this classification is not so accurate the analysis of erythropoiesis remains unsolved.
In the present study, the classification of human erythroblasts was made according to karyometry and autoradiography by which the setting of erythroblast compartments had been determined in rabbit bone marrow.
The mean nuclear diameter of each erythroblast compartment of man was determined as follows;
compartment I: 11.3μ, compartment II: 9.6μ,
compartment III: 8.2μ, and compartment IV: 7.0μ.
In patients with iron deficiency anemia the presence of ineffective erythropoiesis was detected in the compartment III and IV.
Moreover, it was asserted that the lack of iron influenced even on the cell diameter of compartment II, and the decrease in heme content of erythroblasts was much more pronounced than that of peripheral erythrocytes.

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Experimental (rabbit) and clinical studies were carried out on the bone marrow toxicity of chloramphenicol (CP) and thiophenicol (TP).
In the experimental studies, slight inhibition of hematopoiesis, which was characterized by the delayed plasma iron clearance, decreased red cell iron utilization and decreased erythroblasts in the bone marrow smears, was noted in the drug-treated groups. However, despite of the long term treatment with the large doses of both drugs, anemia, leukopenia or thrombocytopenia was not observed.
In the clinical studies, although slight fall of reticulocyte count was demonstrated during CP or TP administration, discontinuance of the drugs reresulted in its quick rise.
Effect of sera from the patients receiving CP on the heme synthesis was determined in vitro by Krantz's method. Minimal or no inhibitory effeect was observed in almost all treated sera except those from patients with liver cirrhosis.

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A case of leukemic reticulosis was reported.
Patient was a 36-year-old female. Her initial symptom was severe anemia. She had neither lymphadenopathy nor hepatosplenomegaly. Bone marrow punctures of the sternum and ilium showed a remarkable proliferation of reticulum cells. Four remissions were obtained following repeated treatments with various anticancer drugs and adrenocortical hormone.
At autopsy, diffuse infiltrations of reticulum cells were found in the bone marrow, lymph nodes, spleen, liver, kidneys, heart, uterus, etc. But tumor formation was scarce.
Discrimination of leukemic reticulosis and leukemic reticulosarcomatosis was discussed.

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A 60-year-old male with multiple myeloma was reported. He had extensive extraosseous lesions. The site of tumor infiltration included liver, spleen, subclavicular lymph nodes, adrenal glands and retroperitoneal space. Biophysical examinations revealed that proteinuria of this patient contained Bence-Jones protein in different molecular size. Cyclophosphamide and prednisolone treatments were successful in controlling the excretion of Bence-Jones protein.

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Two-year-and-4-month-old boy with congenital afibrinogenemia was investigated mainly in regard to the microdetermination of fibrinogen in plasma.
Although the determination of the trace of fibrinogen was unsuccesful by the method of blood coagulation, electrophoresis or immunoelectrophoresis, by means of the hemagglutination inhibition test. The amount of plasma fibrinogen in this case was measured to be 4.2 mg/100 ml.
It may be mentioned that the hemagglutination inhibition test is one of the most hopeful method to detect very small amount of fibrinogen in case of congenital afibrinogenemia.

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A case of von Willebrand's disease was reported. The patient, 20-year-old female, was pointed out the prolongation of bleeding time in the pre-operative examination for tonsillectomy. She was admitted to Tokushima University Hospital for detailed examination of the bleeding tendency.
There was nothing in a personal or family history to suggest a bleeding symptom. Hematological examinations were within normal limits except slight disturbance of megakaryocyte maturation In coagulation tests, whole blood clotting time, platelet count and clot retraction showed normal values, however capillary resistance, prothrombin consumption, platelet adhesiveness or aggregation, plasma or platelet factor in T.S.T. were decreased. Factor VIII activity revealed 25% of normal, which increased to more than expected value after a transfusion of normal fresh blood.
Administration of adrenochrome resulted the shortening of bleeding time and disappearance of purpura.
Coagulation tests were also done in her mother and brother. and the genetic basis of this disease could be suggested.
Aspirin tolerance test in this disease, described by Quick, was discussed.

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The patient was a 10-year-old girl who noticed the enlargement of left cervical lymph nodes in April, 1965. She was admitted to our hospital in November, 1966 and diagnosed as stage IV, -B of Hodgkin's Disease. The histologic type of the lymph node was nodular sclerosis. She received radiotherapy, chemotherapy and corticosteroids but her general conditions became gradually poor. One week prior to death she complained of abdominal pain and dyspnea. Dyspnea was increased and she died on July 14, 1968.
Autopsy revealed secondary disseminated cryptococcosis. Cryptococcosis has been described as a common complication of patients with Hodgkin's Disease. The factors in the etiology of this complication were discussed.

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Since Lorenz and Quaisar first described a case of panmyelopathy following hepatitis in 1954, twenty-nine cases have been reported.
With three exceptions, all the patients were young and most of them were male. In almost all cases, pancytopenia developed after the hepatitis had subsided and all but eight patients died.
In our two patients pancytopenia developed ten and twenty-six weeks after the onset of hepatitis and death occurred ten and twenty-four weeks after the onset of pancytopenia.
In both cases the hepatitis was improving at the time of death. In our cases toxic effect on the liver of benzol or chloramphenicol preceded that on the hematopoietic system would be considered; in one of them, an autoimmune mechanism was suggested to explain the development of pancytopenia following hepatitis.

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