Recently disturbance in lipid metabolism has become an important problem for the study of arteriosclerosis, the excessive lipid in blood being considered both experimentally and clinically as a cause of this disease. Since Hahn found that heparin cleared alimentary lipemia in the body, many studies have been made on the behavior and nature of an active serum substance ("Clearing factor" by Korn et al.), which is produced by the intravenous injection of heparin. With the advance of analytical techniques such as ultracentrifugation and paper-electrophoresis, a new idea has been introduced concerning blood lipid, and the clearing factor is now considered closely related with lipemia and the restoration of the normal lipoprotein. Since the quantitative determination of the endogenous clearing factor is difficult at present, experimental studies were carried out on the post-heparin serum clearing factor and on its relationship to atherosclerosis.1) Serum factor required for the production of the clearing factor was contained in a large amount in α-globulin.2) A large proportion of the clearing factor in the serum, formed after the intravenous injection of heparin, tended to be contained in serum albumin fraction.3) Between the clearing factor and antithrombin II, which both are increased after the in-_travenous injection of heparin, there were evident differences in the time of appearance after heparin injection, the behavior against inhibitors, the thermostability, and the distribution in serum protein fraction.4) The formation of the clearing factor by heparin was investigated with various human organs removed at autopsy, and the formation was found increased in the order : The aorta, kidney, liver, spleen, pylorus, heart, lung, and pancreas. No organ specificity was found for the clearing-factor-forming ability. This ability was found decreased in tissues with marked arteriosclerosis.5) The ability declined with advance in age, more remarkably in the male. In the female no such decline was observed before the age of 40 years. When age and diseases were disregarded, mean value of the clearing factor was rather higher in man than in woman.6) The ability was lower in hypertensive group than in the normal.7) When the normal and abnormal electrocardiographic groups were compared, the ability was lower in the latter, which presented abnormal RS-T segments. 8) The ability was lower in cases with high atherogenic index than in the normal.9) When various diseases were compared, the ability was remarkably decreased in angina pectoris, myocardial infarction, diabetes mellitus, cardiac asthma, and hypothyrodism.

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In experiments with 10 dogs the author took direct lead E.C.G. simultaneously over the intra vena cava superior of its initial region and the atrial surface, and calculated the activation times at different points on the atrial surface, taking for the activation times to lead points what were expended between the initial point of the P wave led from the intra vena cava superior and where the intrinsic deflection of the P wave led from the atrial surface crosses the zoro-line. Then the author obtained the results that is showed in figure 1-4 and table I, and considered the formation of the stimulus conduction in the atrium in deference to these results. There are experiments of like nature by Lewis, Sodi-Pallares and others. However, as I found some points in their reports that I couldn't agree to, I have here brought about some comments on their opinion.The summary and conclusion of this study are as follows : 1) The initial stimulus point coincides with the anatomical region occupied by the head of the sinus node ; and the P wave in the unipolar lead E.C.G. led from that point is always found to be a negative wave of QS type.2) The activation values brought forth by the author for the different points on the atrial surface correspond to those of Sodi-Pallares. But the fact that the values are not in proportion with the distance between above said points and the head of the sinus node can hardly be explained by Sodi-Pallares's theory in which he says the stimulus conduction in the atria is of the nature of diffusion. The author deems it more reasonable to explain the fact by accepting the assumption that there exists a stimulus conduction pathway in the atria.3) The main pathways are assumed to be such as ; (i) one coming downward from the head of the sinus mode along the taenia terminalis toward the vena cava inferior ; (ii) one proceeding from the middle part of the sinus node descendens of the middle of the anterior wall of the right atrium toward the vena cave inferior ; (iii) one which branches off the above mentioned pathway on its way ascending the middle part of the right atrium toward the right appendage : (iv) one coming directly from the head of the sinus node toward the left atrium through the Bachmann's bundle ; (v) one which branches off the Bachmann's bundle descends the anterior wall of the right atrium along the region bordering the septum. Stimulus conduction all over the atria is assumed to be carried out through a number of pathway that have branched off the above said main pathway.4) The form of P wave in the unipolar lead E.C.G. of the atrial surface has no definite relation with activation time.5) Of all the atrial surface the region where stimulus arrival is the latest is a place in the posterior wall of the left atrium near where it borders the ventricle.

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In order to study the renal function in chronic renal failure, I examined renal clearance of nitrogen, creatinine, sodium, chloride and potassium in early morning and water diuresis in patients with chronic renal failure, and compared with the results in compensated stage of chronic nephritis.In water diuresis the excretion of nitrogen, sodium, chloride and potassium increased in compensated stage of chronic nephritis, while little change was noted in chronic renal failure.In chronic renal failure, renal tubular reabsorption of water, sodium chloride, potassium and nitrogen was markedly decreased as glomerular filtration rate was decreased; in severe case of chronic renal failure potassium excretion was exceeded the filtrated volume in glomeruli, that may mean the tubular excretion of potassium.The excreted load of nitrogen in each nephron was calculated as N/GFR, which was markedly high in chronic renal failure, and showed significant relation between the lowered reabsorption rate of water. In chronic renal failure significant relation was found between the lowered sodium reabsorption rate and N/GFR both in water diuresis and in early morning, while in compensated stage of chronic nephritis the relation was noted only in water diuresis. The relation between the reabsorption rate of water and that of sodium was observed in water diuresis in either group, and only in early morning of renal failure group.With the results obtained, it may be acertained that in chronic renal failure as the glomerular filtration rate decreases the excreted load per nephron increased, which causes the osmotic diuresis and lowered reabsorption of water and sodium. However, as the total excreted volume of sodium changes little, the lowered reabsorption of sodium may not mean the lowered reabsorptive function, but it should be considered as the adaptive functional pattern of kidney with decreased nephron.

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Studies obtained on blood concentration of quinidine in the treatment of auricular fibrillation, were as follows : 1) With a single oral dose of 0.4 gm. of quinidine sulfate, the peak of the level was obtained in one to four hours, and content in blood at its highest level in each case was from 1.9 to 5.2 mg, per liter. There were considerable variations of blood concentration of quinidine, not only among individuals but also day by day in the same patients.2) In cases in which a single dose of quinidine was given orally, the blood level increased more rapidly and then decreased more slowly. Average proportion of blood level to the peak level at various times was 23.4 per cent 3 hours before the peak, 43.3 per cent 2 hours before the peak, 72.5 per cent 1 hour before the peak, 80.9 per cent 1 hour later, 66.7 per cent 2 hours later, and 54.3 per cent 3 hours later.3) Blood concentration of quinidine has no exact relation with ff interval, so that it is impossible to judge its effect on the heart through blood concentration of quinidine.4) When quinidine was given repeatedly at 4 hours intervals, its average concentration in the blood 24 hours after drug administration was 4.7 mg. per liter with each dose of 0.4 gm ; 2.8mg. per liter with each dose of 0.3mg ; and 1.0mg. per liter with each dose of 0.2 gm. Quinidine blood level was higher when large doses of quinidine was administered within a short period.5) Individual varation of blood concentration of quinidine was measured in definite schedule of its administration. When 0.4 gm. of the drug was given at 4 hours intervals, the blood concentration showed 2.2 to 9.0 mg. per liter 24 hours after the beginning of the treatment.6) In 36 cases (40 times) of chronic auricular fibrillation, in which conversion to sinus rhythm occurred, the blood concentration was 0.8 to 10.5 mg. per liter. This concentration was related to cardiac enlargement, but not to age and duration of auricular fibrillation.7) The administration of 0.4 gm. of quinidine at 4 hours intervals may be the most suitable procedure for the constitutions of the Japanese.

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Results of quinidine therapy in 63 cases of auricular fibrillation were as follows : 1) Successful restoration of sinus rhythm with quinidine was obtained in 54 out of 63 cases of auricular fibrillation (86%) ; in 46 out of 55 chronic cases and in all 8 cases of paroxysmal auricular fibrillation.2) In chronic auricular fibrillation, successful restoration was obtained in 22 out of 24 cases of arteriosclerotic and hypertensive heart disease (92%), and in 21 out of 28 cases of mitral valvular disease (75%).3) Long duration of auricular fibrillation does not preclude successful treatment. Age of patients and f wave have no relation with the successful restoration of sinus rhythm. On the other hand, success is less likely in the presence of enlargement of the heart and congestive heart failure in the past and present.4) Results of quinidine treatment was so superior in large doses within a short period, that 13 out of 15 failures were improved by administering less than 0.3 mg. at 4 hours intervals.5) Methods of quinidine administration were related to time for the successful restoration of sinus rhythm ; in large doses, sinus rhythm was obtained within relatively short periods.6) There was no relation between the total amount of quinidine required to convert to sinus rhythm and associated diseases, complication of congestive heart failure, duration of auricular fibrillation and f wave formation.7) During quinidine therapy there were 2 cases of ventricular flutter or fibrillation, and 3 cases of embolism, and one case of death in each group.8) Of 43 cases which had been restored of sinus rhythm, with or without maintenance doses of quinidine, relapse occurred in 67% one year later, and in over 2 years, only 7% of cases has sinus rhythm. Relapse occurred in 17 out of 20 cases with mitral valvular disease (85%), and 9 out of 20 cases with arteriosclerotic and hypertensive heart disease (45%). In 14 cases in which sinus rhythm was maintained, 13 cases need of less than 3.0 gm. of quinidine in total to convert the sinus rhythm.

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