Fukutome and his collaborators¹⁾²⁾ reported that the growth of mutabiles of E.coli was inhibited by galactose and that this phenomenon could be used as a bioassay of galactose.
We intended to study the availability of such kind of bioassay for galactose tolerance test in liver function tests. If the inhibitory effect of galactose is not influenced by the coexistence of glucose, we can measure the blood level of galactose without the differentiating analysis of that from glucose (fermentation procedure). Although glucose of a concentration higher than some level reduced very much the inhibitory effect of galactose on the growth of mutabiles, we could find the conditions where the influence of glucose could be neglected and the measurement of galactose could be performed without any fermentation procedure.

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Constitutional hepatic dysfunction showing an increase in the free form of the plasma bilirubin, was first reported by Gilbert¹⁾ under the term of "cholémie simple familiale" in 1901. Similarly in 1948, Rotor²⁾ reported the other type of constitutional hepatic disorder which showed mainly an increase in the conjugated form of the plasma bilirubin. However, histological examination of the liver in these two types of diseases has been reported to be within normal limits. In 1954, Dubin and Johnson³⁾ described another type of the disorder under the term of "chronic idiopathic jaundice with unidentified pigment in the liver cells" which showed characteristic pigment in the liver cells and an increase in the conjugated form of the plasma bilirubin.
These three disorders have many problems yet to be dissolved. In Rotor syndrome, despite of quite similarities to Dubin-Johnson syndrome in clinical and laboratory findings, there has been no report in which the confirmation of the pigment in the liver was made. These made us to study the two conditions with an use of electronmicroscope to find whether they are the same or different in their etiology and to delineate the particular pigmentation in the liver of Dubin-Johnson syndrome, as to its origin or nature and difference from ordinary brown colored pigmentation in the liver seeing in cases of cirrhosis, hepatitis or even in normal cases. In addition, we studied the cases of Gilbert's disease under the same circumstances.

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The present report deals with the studies on the epidemiology, etiology, diagnosis, clinical pathology and treatment of thyroid diseases in my clinic.

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At the beginning of this presentation, the pulmonary hypertension was classified into three groups as follows :
1) Pulmonary pulmonary hypertension
2) Pulmonary hypertension in congenital cardiovascular disease
3) Pulmonary hypertension due to the left heart disease
This (3) pulmonary hypertension due to the left heart disorder corresponds to the passive pulmonary hypertension (Wood, P.) and is accompanied by the elevation of the pulmonary venous pressure. Pulmonary hypertension due to left to right shunt in congenital cardiovascular disease (2) is equivalent to the hyperkinetic pulmonary hypertension. And pulmonary pulmonary hypertension (1) is caused by the disease of the lung and/or thorax and has possibility to develop the pulmonary heart disease defined by WHO.

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This report has dealt with the cardiopulmonary function of the patients with cardiac dyspnea in attempt to confirm the appearance of bronchoconstriction in the seizure of cardiac asthma.

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This investigation was supported by a Public Health Service Research Grant (HE 08018) from the National Heart Institute, U. S. Public Health Service.

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