A new small portable viscosimeter, cylinder type was developed, in which viscosity of blood was transformed into electric signal on the inner surface of cylinder and recorded automatically after being amplified.
With this viscosimeter coagulation process of blood was recorded and its coagulation curve obtained, made possible an accurate analysis on blood viscosity, particularly in the process of coagulation.
By this technique the effect of Reptilase was observed to find that this agent shortened the coagulation and elevated the maximum viscosity, and also its activity was enhanced by carcium ion.
In vivo studies, intravenous injection of 2ml of Reptilase accelerated coagulation and at 30 minutes after injection its effect reached to the maximum and remained for 2 hours.

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There have been only a few informations about the effects of Trasylol on the dynamic balance of the coagulation-fibrinolysis system, and the precise mechanism of the effects has not been wholly elucidated. This report presents the data of in vitro, in vivo, and clinical studies on the effects of Trasylol on the coagulation-fibrinolysis system.
Results:
1. In vitro experiments;
Trasylol inhibited the activities of plasmin and plasminogen activator in fibrinolysis, and prolonged PTT in coagulation.
2. In vivo experiments;
Trasylol possessed inhibitory effects on the fibrinolytic enzyme system (STT shortened, HIT depressed), and on the 1st phase of blood coagulation (PTT prolonged).
3. Clinical studies;
Trasylol when administered in 12 patients for the purpose of hemostasis, presented significant effects in 3, good effects in 3, and no effect in 6. STT was proved to be very useful for the estimation of activated fibrinolysis.

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In order to obtain the number of the white blood corpuscles in 1.0 mm³ of blood by way of Thoma's counting slide which is now used, we count the number of the white blood corpuscles in the chamber of 1.0 mm² of the base area by 0.1 mm high.
The (demanded) height being 1.0 mm, we must multiply the figure obtained in the above-mentioned method by 10, and by the ratio of dilution, again.
Therefore, when the blood is diluted by the ratio 1:10 with Türk's liquid, one white blood corpuscle under the microscope equals 100 corpuscles as data.
Any trivial error caused by the improper handling of the slide or oversigh under the microscope makes a serious error.
To decrease these kinds of errors, I turned the chamber into a new one with the base area 10.0 mm² (2.0 mm×5.0 mm) by 0.1 mm high, and on the surface of it I gave the section which make it easy to count the white blood corpuscles.
Accordingly, one corpuscle under the microscope is equal to 10 data, and so we can get a more correct number.
Besides, I made such an improvement on the chamber as would make it easy to count the red blood corpuscles.

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A 38-year-old male was hospitalized to the Tokyo Medical and Dental University on June 17, 1966 with a complaint of dyspnea. About a month previously he was admitted to another hospital complaining of dyspnea, and was found to have a marked anemia, leukocytosis of 388,000/cmm. and bilateral massive pleural effusion. Prednisolone therapy had been started with a diagnosis of acute leukemia before he was referred to the authors.
Physical examination on admission showed marked palor, generalized petechiae and slight lymphadenopathy. There was no hepatosplenomegaly. Blood study revealed hemoglobin 5.2 Gm./dl., Leukocyte 3,300/cu. mm. with 21 per cent leukemic cells and occasional erythroblasts, and platelet 12000/cu. mm. The bone marrow was dominated by leukemic cells of lymphoblastic type. Erythroblasts both in the peripheral blood and bone marrow were normoblastic. A prominent accumulation of fluid was proved in bilateral pleural cavities on chest x-ray. Examination of the effusion revealed 2,700 nucleated cells per cmm., of which 53.2 per cent was consisted of leukemic cells; 12.4 per cent, of myeloid cells; and 13.2 per cent, of erythroid cells. Some of the last cell group showed megaloblastoid characteristics. The cytological characters were also seen in the effusion of both pleural cavities. Coenzyme B₁₂ and folic acid were instilled into the pleural cavity without any effect either on the counting or morphology of megaloblastoid cells in specimens obtained after 6 and 24 hours Biopsy of the parietal pleura disclosed no focus of hemopoiesis, but only a slight leukemic cell infiltration.
Following the VAMP treatment the patient retained incomplete remission for about two months, in which the pleural effusion gradually decreased and disappeared. He died on October 21, 1966 in relapse. Autopsy disclosed a marked leukemic infiltration in various organs and tissues, particularly in bone marrow, lymph nodes, liver and pleura. No extramedullary hemopoiesis was found in any organs or tissues throughout the body.
Although extramedullary hemopoiesis could not be detected on examinations either post or ante-mortem, there might have existed such foci in the pleura or its neighbouring tissues in view of the variety of hemopoietic cells in the pleural effusion. The etiology of the megaloblastoid changes however, remained obscure.

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A 9 Year-old boy was admitted to Toho University Ohashi Hospital complaining of hemorrhagic diathesis.
In March 1959, he was admitted to another hospital with the chief complaints of one year long sever epistaxis. Prednisolone and blood transfusion therapy was started under the diagnosis of ITP. As hemorrhagic tendency continued in spite of the admission treatment, he was transfered to our hospital for further evaluation on October 22. 1965. Physical examination on admission revealed the slight epistaxis and several petechiae. Laboratory findings: ESR 7 mm/h, Hb 64%, RBC 345×10⁴, WBC 4700, Ret 32‰, Ht 38%, platelet 4.1×10⁴, Prolonged bleeding time, positive tourniquet test and impaired prothrombin consumption and clot retraction. The number of megakaryocytes was extreamly decreased, no LE cells. Platelet antibody was observed.
After first admission, platelet transfusion was performed five times without any effect. Prednisolone treatment was continued two monthes with moderate effect.
After discharge (Dec. 1965) his hemorrhagic tendency was not disappeared in spite of prednisolone treatment.
On may 16. 1967, he was readmitted to our hospital. Splenectomy was performed on July 7, 1967, because of no effect was expected by 6MP treatment (1 mg/kg/day).
The histology of the spleen revealed marked fibroadenia.
After the operation platelet count was not increased, nevertheless hemorrhagic diathesis was tremendously disappeared.

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Four cases with plasmacytoma-like bone marrow findings are presented. Clinical diagnosis of them were agranulocytosis, Banti's syndrome, Pulmonary tuberculosis with aplastic anaemia and Grawitz's tumorrespectively.
Monoclonal gammopathy, Bence-Jones proteinuria and osteolytic lesions were not found in these cases. The plasmacytic elements in these cases were 1.0 to 47.8% and large abnormal plasmacytes were observed.
Reactive plasmacytosis must be differentiated from plasmacytoma, but occasionally it is very difficult at present time. Further observation seems to be necessary to accomplish that.

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In six cases with the chronic occlusive arterial disease, the transient hypofibrinogenemia was observed in their clinical courses.
1) The diminution of the plasma fibrinogen level was noted only in cases with inflammatory arterial diseases.
2) Although the plasma fibrinogen level was abnormally low, the hemorrhagic tendency was observed only in one case.
3) There were neither reduction of fibrinogen producing activity, such as in liver disease, nor progression of fibrinogen destruction, such as in blood dyscrasia, septicemia and malignant tumor.
4) The palsma fibrinogen level decreased with exercerbation of the arterial disease and returned to normal with the improvement of the pathologic process.
Based upon these findings, it is suspected that the transient hypofibrinogenemia observed in our cases has some relation to the inflammatory arterial diseases.

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A rare case of multiple myeloma accompanied with extramedullary plasmacytomas in the skin and muscle was reported. The patient, 46-year-old female, was first admitted on September 18, 1965 complaining of the swelling and pain in the left mandibular region. The diagnosis of type L G-myeloma was established. She responded to treatment with cyclophosphamide and was discharged on November 27, 1965. The patient was rehospitalized on January 31, 1967 because of a firm, smooth, tender mass over the sternum. The tumor diminished in size by x-irradiation and almost disappeared, when a nodule was found in the skin of the left paresternal area adjacent to the first tumor. Thereafter, similar nodules developed one after another in the skin of various parts of the body. Although the nodules were supposed to be radiosensitive, application of x-irradiation was limited to some of them because of radiation pneumonitis. Chemotherapeutic agents such as ibenzmethyzine, cyclophosphamide, urethane and Toyomycin were inefiective against the nodules, nine such lesions being left when she died on August 29, 1967. Autopsy disclosed that the nodules were extramedullary plasmacytomas developed in the subcutaneous fat tissue, muscle and lymph nodes.

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A case of “hemolytic uremic syndrome” occurring in a patient with paroxysmal nocturnal hemoglobinuria was described. The patient was a 29-year-old female presenting with symptoms of acute hemolysis, marked thrombocytopenia and acute renal failure, which started following upper respiratory infection, abdominal pain and diarrhea. A decrease in factor V, factor II and fibrinogen, as well as a prolongation of whole blood clotting time and prothrombin time, was associated with the development of “hemolytic uremic syndrom.” Euglobulin lysis time was within normal limits. The characteristic finding in the hematological examination was typical fragmentation of the erythrocytes seen on the blood film. The patient died in spite of the anticoagulant therapy with heparin. Necropsy revealed disseminated thrombi in several organs such as brain, lung, stomach, duodenum, liver, spleen and kidney. No renal cortical necrosis was observed. The local impairement of microcirculation following vascular thrombi in the kidney was considered as a cause of the acute renal insufficiency. It is suggested that “hemolytic uremic syndrome” is one of the manifestations of consumption-coagulopathy.

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The Patient was a 11-year old girl who was apparently well until Jan., 1966 when she noticed anemia and hemorrhagic diathesis. These became progressively worse. A diagnosis of acute granulocytic leukemia was given on March 27, 1966 when she visited the Gunma University Hospital and was admitted to the Jomo-Chuo-Byoin.
After transient partial remission induced by treatment with prednisolone and antibiotics, anemia developed again and the left neck lymphnode enlarged. The elarged lymphnode was softened and a fistula was left after drainage. Because of increase in leukocyte count and enlargement of the right inguinal lymphnode refractory to the additional treatment with 6MP, she was transfered to the Gunma University Hospital on the 141st hospital day. After the admission to the Gunma University Hospital the right neck node diminished its size and the fistula was closed spontaneously. However, general condition was getting worse. She complained precordial pain and right sided chest pain from the 185th hospital day. Physical examination revealed pleural friction rub and pleural effusion in addition to a small amount of ascites fluid. X ray of the chest revealed a moderate right pleural effusion and enlarged cardiac shaddow. Low voltage was characteristic finding of EKG at that time. Protein concentration of the ascites fluid was initially 1.8 g/dl. It increased to 3.0 g/dl with positive Rivalta reaction. The pleural fluid and ascites fluid remained steril to routine and acid fast cultures. Most of the cells in the fluid were myeloblasts or promyelocytes. She died on the 205th hospital day. Autopsy revealed both leukemic pericarditis and pleurisy. Two abscess were present in the liver and the intestine was adhered each other. Histological examination of the intestinal serosa revealed a significant infiltration of the inflamatory cells in addition to that of the leukemic cells. The genesis of polyserositis observed in this patient was discussed.

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