Since the original description of arachnodactylia by Marfan 1896, about 280 cases of this disease have been reported, of which about 40 cases are found in Japanese literatures.
The auther observed a patient, who showed a typical Marfrn's syndrome.
The patient was an unmarried japanese man, aged 31 years. Nothing noteworthy was found in his past history except for abnormal body form. In June, 1948, illness began with severe agonizing, compressing pain over the anterior chest and the right back, accompanied with palpitation and dyspnoea.
In October, 1948, the patient was transferred to our hospital.
Physical examination revealed as follows- His height was 175.6 cm (taller than common japanese man), and his weight was 56.0 kg. His extremities were slender and long, and showed typical arachnodactylic forms. Disharmonious bodily development, dolichocephalic head with old-appearing features, lordoscoliosis, pes planus, and hallux valgus were marked. Vision was short sighted. No dislocatio lentis.
The heart was markedly enlarged, rough systolic and diastolic murmurs were loudly heard over the entire precordium, and they were most intensive at the aortic ostium. (aortic steno. insufficiency and mitral stenoinsufficiency) Electrocardiogram showed the existence of myocardial disturbance.
Roentgenologic examination revealed marked aortic aneurysm.
The blood pressure was 117/45 in the right arm, 131/33 in the left arm.
The blood Wassermann was negaiive. There was a marked pulsation over the middle abdomen. Palpatoric finding and roentgenologic examination revealed aneurysm of aorta abdominalis.
Sella turcica was shallow and very small. Long tubural bone showed remainning epiphyseal line and pseudo-epiphyseal formation. These findings may prove the existence of endocrine dysfunction. Hematologically nothing was abnormal, except for eosinophilia (8.0%). Neurologically normal.
In this case familiary relationship was evidently recognized. Bloodrelational appearance of this disease showed Menders dominat hereditary type.
Except for a attack of asthma cardiale, the patient was almost asymptomatic during his hospital stay.
On December 3., 1948, he was sent home. In the middle of December, 1948, symptoms of decompensation rapidly developed, and he died suddenly on December 23., 1948.

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From what has been reported in medical literature, it is assumed to be true that the quantity of glycogen presented in tissues and organs do vary in accordance with the type of tissues and the kind of animals, and there is no unanimity of reaction of these animals in the content of glycogen in tissues and organs toward either insulin or adrenalin even though the shortcoming of the study procedure heretofore in use which disregards individual variation of glycogen content in tissues and organs have been corrected.
The author, therefore, attempted to observe the influence of either insulin or adrenalin on the intermediate sugar metabolism with the use of rat as the experimental animals based on the following points:
1. In order to find out the actions of insulin or adrenolin on the carbohyddrate figures in general of the liver and extrahepatic tissues (skin and muscle), the determination made of the changes on carbohydrate figures, glycogen contents, free sugars and hydrolysable sugars of rat's liver and extrahepatic tissues (skin and muscle), upon the administration of insulin or adrenalin, following Yamamoto's method.
2. To ascertain causes to show the difference in their reaction of respective carbohydrate figures of tissues and organs of animals toward insulin or adrenalin, the quantitative deter. mination on the activity of diastatic ferment of livers, muscles and skin of rat were undertaken. While, several diastatic ferments of organs can be mentioned, as concerned with glycogenolytic activity of enzyme, its evaluation was based on Nakahira's method, which consists of a procedure which a certain definite quantity of glycogen was used as a substrate, with an addition of a certain quantity of macerated tissues, and the quantitative determination of decompose substrate at a regular interval.
The Experimental Results were summarized as follows:
1. In insulin mice, blood sugar and free liver sugar were markedly decreased in the initial stage, then, there occurred decrease of liver glycogen and in the succeeding stage the decrease of free sugar in muscles and skins noted. In this stage, the glycogenolytic activty of ferment had been remarkably suppressed.
2. With adrenalin, liver glycogen has decreased, but blood sugar had increased adversely parallel with the decrease. Glycogen decrease occurred next in muscles and skins, here, no change observed in glycogenolytic activity of ferment in blood, tissues and organs.
3. From these findings, the main reaction seen in insulin rat was the lowering of free sugarin tissues and organs, and in adrenalin rat the lowering of glycogen occurred in the first stage. Then, in insulin rat the suppression of glycogenolytic activity of ferment seen but with adrenalin, there was no change in glycogenolytic activity which speaks for possible linking of intimate relations which may present between glycogen of tissues and organs, and their glycogenolytic ferment. (Auther's abstract)

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In diabetes caused by injecting alloxan into rabbits, I observed on the combined sugar of each phase after the injection of alloxan and on the changes of the combined sugar in glucose tolerance and Insulin tolerance.
1) The combined sugar increased almost in the initial hyperglycemic, the hypoglycemic and the diabetic phase. But most of cases in rabbts led to death when the combined sugar decreased in the hypoglycemic phase.
2) In a insulintolerance of alloxan dibetes in rabbts I had the following data the combined sugar showed the greates increase in one hour after the injection of alloxan, but its increasing degree was less than the control.
3) In glucose tolerance, however there were various types, most of combined sugar had the tendency to decrease markedly in one hour after the injection of alloxan, but the control had the tendency to increase.
4) Most of alloxan diabetes in rabbits is, prof. Iizuka had already introduced in human diabetes, panhyperglycémie, and the other Hyperglycémie normoproteidoglycemique or Hyperproteidoglycémie normoglycemique.

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The rabbts were divided into 4 groups: (1) the control (2) two hours,(3) four or five hours, after the injection of alloxan, especially in an attack of a hypoglycemic shock (4) diabetic phase after 48 hours. Rabbts were gived alloxan (generally 200 mg/kg) intravenously following 48 hours fast, and liver glycogen, muscle giycogen and heart glycogen were determined in each phase.
1) Liver glycogen decreased in the initial hyperglycemic phase, came to its contain of normal rabbit in the hyoglycemic phase. Liver in the diabetic phase contained markedly less glycogen than normal rabbit liver.
2) Muscle in the initial hyperglycemic and the diabetic phase contained less glycogen than normal rabbit muscle, especially markedly in the hypoglycemic phase.
3) The fluctuation of heartglycogen was very interesting. Heart in the hypoglycemic phase contained more glycogen than normal rabbit heart, especially markedly in the diabetic phase.

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I studied on the protein intermediate metabolism by KJO₃ method in each phase following the injection of alloxan.
1) The KJO₃ value of serum tended to increase in the initial hyperglycemic and the hypoglycemic phase, but to come to normal or to decrease in the diabetic phase.
2) There was no special relation between blood sugar and KJO₃ value of serum after the injection of alloxan.
3) There was a parallel relation between combined sugar and KJO₃ value of serum after the injection of alloxan.

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