Sample of scalp hair obtained from 81 healthy male subjects ranging in age from 2 to 91 years were washed with methanol and kept hydrated with distilled water. The diameter was determined with micrometer under a microscope, the breaking strength, the rate of extension upon breaking, the work upon breaking, and the Young's modulus in the rising phase were measured with Tensilon III apparatus. Diameter of the hair, ranging from 60 to 140 micron, rose until the age of 15, followed by a gradual decrease with advancing age.
Breaking strength and work upon breaking also showed similar tendency. Young's modulus was decreasing until the age of 20, followed by a gradual rise ithw advance in age. These physical properties of human hair appears to be useful as indices of aging.

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An aged man who had signs suggestive of portal hypertension and hypersplenism, showed hepatic fibrosis without splenomegaly at autopsy. Discussion was made on a relationship between portal hypertension, hypersplenism on the basis of senile change of the spleen.
A 75-year-old man was admitted to the hospital complaining of a massive hematemesis of 500ml in April, 1966. He was a deaf mute. Liver and spleen were not palpable, and marked as cites was noted. Upper gastrointestinal series showed varices at the lower portion of the esophagus. Tentative diagnosis was cirrhosis of the liver, and he was treated with diuretics and discharged. The patient was readmitted to the hospital due to aggravated ascites in December, 1966. Hemogram showed a red cell count of 3.4 millions, a white cell count of 3, 300, with 75% neutrophils and thrombocyte count of 80, 000. Total protein was 7.2g/dl, A/G ratio 0.57, icterus index 25, BSP test 35%, alkaline phosphatase 6.0 units (Bessey), S-GOT 20 units and S-GPT 50 units.
His clinical course was intractable to the diuretic therapy, and complicated by remittent fever, anemia, leucopenia, and thrombocytopenia. He died of a recurrent bout of hematemesis.
Autopsy revealed 3.5l of ascites, remarkable varices at the lower end of the esophagus, 3.0l of fresh blood in the stomach, and tarry stool in the intestine. Liver was 840g showing a considerable periportal fibrosis with some porto-central septal formations without any regenerative processes. Some small portal veins were completely obliterated with monocytic infiltration. Chronic cholecystitis was found and coliform bacilli were positive by the bile culture. The spleen was 130g and showed marked perisinusoidal fib rosis and fibrinoid degenerations on the walls of small arteries.
The case was suggestive of hypersplenism clinically, but there was no splenomegaly at autopsy. Senile change of weight of the spleen among a total of 492 cases showed a tendency to decrease with aging. The weight of spleen in this case was located on the upper normal limit, which suggested some influences of senile atrophy of the spleen to explain the absence of splenomegaly. But spleen in Banti' syndrome was not tenable because of absence of sinus hyperplasia and Gamna-Gandy bodies. In this case repeated chronic cholangitis might have induced interstitial hepatitis, and lesion in the periportal space might have played an important role in the production of portal hypertension and hypersplenism. The case apparently resembled idiopathic portal hypertension, but finally was considered to be fibrosis of the liver or senile cirrhosis of the liver from the viewpoint of senile change of the organs.

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