Utilizing 133-xenon gas and a scintillation camera, we examined the distributional relation between ventilation (V^^.) and perfusion (Q^^.) in patients with pulmonary hypertension (PH) comprising mitral stenosis (MS) and left to right shunt disease (shunt). In the case of MS, Q^^. decreased at the dependent part of lung in proportion to the degree of PH, but preserved normal V^^. and resulted in high V^^./Q^^. value at this region, which was estimated to cause the physiological dead space effect on the gas exchange function. In the case of shunt disease, even with a high degree of PH, reduction of Q^^. at the dependent lung region was not observed with normal preservation of V^^., thus obviating any type of the V^^./Q^^. imbalance. Since the washout of xenon gas by resting tidal volume ventilation was observed to be delayed from the dependent lung region, latent ventilatory impairment in this region due to small air way closure at tidal breathing was also suspected.

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Serum lipoproteins of 25 patients with uncomplicated renal diseases were studied with polyacrylamide gel block electrophoresis. (1) In the nephrotic syndrome (or nephrotic phase of nephritis), marked increase of chylomicrons, pre-beta lipoprotein or beta lipoprotein and decreases of alpha lipoproteins were detected in the most of the patients. Qualitative change was also frequent as in the glomerulonephritis. (2) In the renovascular hypertension, metabolism of serum lipoproteins was involved also. The principal abnormality was in alpha lipoproteins including the lipid-loaded albumin. Marked increase of alpha lipoprotein, was detected in 2 of 3 patients studied in this period. Surgical correction of abnormal physiology had resulted in a return to a normal lipoprotein profile. (3) In the glomerulonephritis confirmed by biopsies, serum lipoprotein abnormalities were detected more frequently than in the reported past studies as analyzed with the method employed in this study. Qualitative as well as quantitative abnormalities were in beta lipoprotein and alpha lipoproteins in the early and middle phase of the disease process. Gross qualitative change occured frequently. Furthermore, lipoprotein abnormalities in renal diseases were reversible; i.e., when the disease had ameliorated or was corrected surgically, the lipoprotein profile returned to the normal or near-normal profile. In conclusion, the results of the present study indicated that serum lipoprotein disorders are involved in the disease process of three major clinical entities of the renal diseases.

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A fine structure of the myocardium was examined in the acute febrile mucocutaneous lymph node syndrome, which was recently prevailing in Japan. The right ventricular myocardial cells in ten cases were observed through endo-myocardial biopsies. On light microscopy, accumulation of histiocytes was demonstrated in some cases. Electron microscopic examinations revealed myofibrillar changes, increased glycogen contents and other degenerative changes. On the myocardium of a case in which a biopsy was performed during the active phase of the disease, these changes were prominent. However, these changes were also observed for some months to some degree.

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The human hear antigens reactive with rabbit antisera to human heart muscle cell membranes were obtained by citric acid extraction of myocardium. Further analysis of heart antigens was performed by DEAE-cellulose column chromatography. Soluble antigens of the streptococcal cell membranes were obtained by hydrolysis of membranes with pepsin. Anti-heart sera were found reactive with the streptococcal antigens and also anti-streptococcal sera exhibited a precipitin reaction with the heart antigens by immunoelectro-phoresis. Furthermore, it was found that after absorption of anti-heart sera with the streptococcal antigens, the precipitating activity with heart antigens could be removed. It might be suggested that a cross-reactive relationship between human myocardium and group a streptococci exists from the immunological evidence.

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Epidemiological studies were performed on the incidence of rheumatic fever and rheumatic heart disease, prevalence of Group A streptococcus and T types of the organisms, and the relationship between the changing pattern of T types and the occurrence of rheumatic fever in Mainland Japan and the Ryukyu Islands. Our results strongly suggested the possibility that the incidence of rheumatic fever is closely associated with the change in T types of streptococcus, rather than persistent, high incidence of the organism in the throat.

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An attempt of PCS was performed for the first time in Japan. Eighteen hundred twenty-six preschool and school children were examined and the result was compared with other studies (physician's auscultation and PCG). The time requirement for a single child is approximately 1.5 min. in primary school. It took long time in kindergarten. The heart murmur detection rate is high and the sensitivity is fairly good, although it is not so good as well-trained physician's heart murmur detection rate. PCS is not perfect, but is fairly good tool for screening. It can be used only by technician. PCS may be able to save the physician's time.

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Two non-rheumatic valvular lesions in which myxomatous degeneration appears to be the genetic or relating factor are described. Floppy valve syndrome of the mitral valve occurs not infrequently in the childhood as well as in the older age, and it should be emphasized that this lesion encountered in the childhood must be carefully differentiated from the rheumatic heart disease. This condition might deteriorate rapidly and bring severe congestive heart failure, eventually with tricuspid insufficiency in spite of intensive medical treatment. The choice of surgical treatment for severe mitral insufficiency is mitral valve replacemnt even in the childhood. Mucoid degeneration is histologically revealed in the aortic valve of patients of ventricular septal defect associated with aortic insufficiency, too. The etiology of aortic insufficiency in this condition previously has been explained to be lace of support structure of the aortic valve.⁴ However, the facts that there may be even an infant associated with severe aortic insufficiency and the aortic valve specimen demonstrates an above-mentioned characteristic feature, would suggest that this condition may be caused by a certain congenital tissue anomaly.

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