The correlation between the plasma insulin, and glucose concentration was studied in healthy Korean adults consisting of 20 males and 22 females of 16 to 38 years of age. The blood samples of above subjects were obtained through cubital vein at arbitrary times, during their usual working hours. Plasma insulin was assayed by means of double antibody system of radioimnmunoassy technics, and blood glucose was determined by means of Van Slyke-Folch method. Results were as follows: 1. There were no differences in the blood sugar levels in relation to the plasma insulin concentration either by sex or age. 2. In the case, when the plasma insulin concentration was within $200m{\mu}D/ml$, the correlation between the insulin, and glucose concentration existed, the ratio of which was expressed as; Plasma glucose concentration(mg/dI)=$91.9+0.08{\times}Insulin$ concentration r=0.62 3. Insulinogenic index was 12.4%, which was somewhat higher than other reports. 4. It is suggested that the correlation between plasma insulin and glucose concentration could be determined at arbitrary times instead of fasting times.

The liver function test was performed by means of two radioisotope tracer techniques in 20 normal subjects and in 63 patients with hepatobiliary diseases. The blood disappearance rates of $^{131}I$-rose bengal and of $^{198}Au$ colloid were determined by external counting method. The hepatocellular function and the hepatic blood flow were estimated from the observed data and the results were compared with those of the conventional liver function tests. The results obtained were as follows: 1. The mean blood disappearance half time of $^{131}I$-rose bengal was $6.6{\pm}0.63$ minutes in normal control, $17.7{\pm}6.93$ in cirrhosis of the liver, $16.6{\pm}4.80$ in acute hepatitis, and $14.7{\pm}3.46$ in obstructive jaundice. It was markedly prolonged in the hepatobiliary diseases as compared with the normal control, but there was no significant difference among the hepatobiliary diseases. 2. The mean blood disappearance half time of $^{198}Au$ colloid was $4.0{\pm}0.66$ minutes in normal control, $9.8{\pm}3.42$ in cirrhosis of the liver, $4.4{\pm}0.82$ in acute hepatitis, and $5.0{\pm}1.42$ in obstructive jaundice. The difference between cirrhosis of the liver and normal control Was statistically significant. However, there was no definite difference among acute hepatitis, obstructive jaundice, and normal control. The mean blood disappearance rate constant (K value) was $0.177{\pm}0.028/minute$ in normal control. In cirrhosis of the liver, it was markedly decreased which was suggestive of the reduced hepatic blood flow. 3. The ratio of $^{131}I$-rose bengal blood disappearance half time to $^{198}Au$ colloid disappearance half time was $1.68{\pm}0.20$ in normal control, $1.82{\pm}0.31$ in cirrhosis of the liver, $3.80{\pm}0.82$ in acute hepatitis, and $3.01{\pm}0.54$ in obstructive jaundice. The ratios in acute hepatitis and obstructive jaundice were remarkably higher than those in normal control and cirrhosis of the liver. 4. There was a significant correlation between the blood disappearance half time of $^{131}I$-rose bengal and that of $^{198}Au$ colloid in cirrhosis of the liver. 5. In cirrhosis of the liver, the blood disappearance half times of $^{131}I$-rose bengal and of $^{198}Au$ colloid were inversely correlated to the serum albumin level. In acute hepatitis, there was a good positive correlation between the blood disappearance half time of $^{131}I$-rose bengal and the serum transaminase activities. In obstructive jaundice, the blood disappearance half time of $^{131}I$-rose bengal was correlated to the serum bilirubin level.

Since the iron balance is maintained by regulated intestinal absorption rather than regulated excretion, there have been many reports concerning the factors which may influence the intestinal iron absorption. As the liver is the largest iron storage organ of the body, any hepatocellular damage may result in disturbances in iron metabolism, e,g., frequent co-existence of hemochromatosis and liver cirrhosis, or elevated serum iron level and increased iron absorption rate in patients with infectious hepatitis or cirrhosis. In one effort to demonstrate the influence of hepatocellular damage on intestinal iron absortion, the iron absorption rate was measured in the rabbits whose livers were injured by a single subcutaneous injection of carbon tetrachloride (doses ranging from 0.15 to 0.5cc per kg of body weight) or by a single irradiation of 2,000 to 16,000 rads with $^{60}Co$ on the liver locally. A single oral dose of $1{\mu}Ci\;of\;^{59}Fe$-citrate with 0.5mg of ferrous citrate was fed in the fasting state, 24 hours after hepatic damage had been induced, without any reducing or chelating agents, and stool was collected for one week thereafter. Serum iron levels, together with conventional liver function tests, were measured at 24, 48, 72, 120 and 168 hours after liver damage had been induced. All animals were sacrificed upon the completing of the one week's test period and tissue specimens were prepared for H-E and Gomori's iron stain. Following are the results. 1. Normal iron absorption rate of the rabbit was $41.72{\pm}3.61%$ when 0.5mg of iron was given in the fasting state, as measured by subtracting the amount recovered in stool collected for 7 days from the amount given. The test period of 7 days is adequate, for only 1% of the iron given was excreted thereafter. 2. The intestinal iron absorption rate and serum iron level were significantly increased when the animal was poisoned by a single subcutaneous injection of 0.15cc. per kg. of body weight of carbon tetrachloride or more, or the liver was irradiated with a single dose of 12,000 rads or more. The results of liver function tests which were done simultaneously remained within normal limit except SGOT and SGPT which were somewhat increased. 3. In each case, there has been good correlation between the extent of liver cell damage and degree of increased iron absorption rate or serum iron level. 4. The method of liver damage appeared to make no obvious difference in the pattern of iron deposit in liver. This may be partly due to the fact that tissue specimens were obtained too late, for by this time the elevated serum iron level had returned within normal range and the pathological changes were almost healed. 5. The possible factors and relationship between intestinal iron absorption and hepatic parenchymal cell damage has been discussed.

The pathogenetic mechanisms of anemia in patients with chronic liver disease were observed. Seventeen patients with moderate to advanced hepatic diseass were studied by various methods. Only patients without previous blood loss were included: 14 had cirrhosis, 2 had active chronic hepatitis, and one had inferior vena cava obstruction with associated liver cirrhosis. The followings were the results: 1. The anemia based on red blood cell count, Hb., and Ht. was found in 76.5-78.6% of the patients. 2. Red cell indices indicated that normo-macrocytic and normochromic anemia was present is the majority of the patients. 3. No evidence of megaloblastic anemia was found on the basis of the morphological examinations. 4. Serum iron, TIBC, % saturation and iron content in the bone marrow indicated that iron deficiency anemia was present in about half of the patients. 5. In the view of the erythrocyte dynamics, primary increase in the red cell destruction was ascribed to the cause of the anemia. 6. Decrease in the red cell survival time was not correlated with MCV, % saturation and S.L. ratio. Also, hemoglobin level was not correlated with MCV, % saturation and $T_{50}Cr$. Therefore, multiple causes may be involved in the pathogenesis of the anemia. 7. Anemia as determined by the red cell volume was found in only 60% of the patients. It may be possible that hemodilutional anemia is present.

The organ distribution study and the whole body scan were done in the albino rats at intervals of 5, 30, 60, 90 and 120 minutes after the intravenous injection of $^{99m}TC$-pertechnetate absorbed in Sephadex beads of $20{\sim}80$ micra in diameter. Effect of additional injection of physiological saline and saline absorbed in Sephadex beads of $20{\sim}80$ micra in diameter on the scan and organ distribution were also studied. The results were as follows. 1. Five minutes after the injection of $^{99m}TC$-pertechnetate absorbed in Sephadex beads of $20{\sim}80$ micra in diameter, Sephadex was well trapped in the lungs, with which the excellent lung scan was obtained. Two hours after the injection, kidneys were well visualized instead of lungs, which suggested that kidney acts as the excretory organ. Five minutes prior to scan, additional injection of physiological saline absorbed in Sephadex above mentioned was done. The bladder was also well visualized together with the kidneys. 2. In the distribution studies, most of radioactivity was detected in the lungs at 5 minutes and was gradually transferred chiefly to the kidneys and bladder and partly to the liver. 3. Additional injection of physiological saline resulted in a rapid transfer of $^{99m}TC$ trapped in the lung to both the kidneys and liver. 4. Additional injection of physiological saline absorbed in Sephadex beads of $20{\sim}80$ micra in diameter resulted in a rapid transfer of $^{99m}TC$ trapped in the lung to only the urinary system. 5. Results of these studies suggested that; a) Other nutrients and therapeutic compounds may be carried into the lungs along with Sephadex beads and then released in high concentration, which would exert greater therapeutic effect locally than that of the usual administration. b) Some radionuclides absorbed in Sephadex could be used as the lung scan agents, the flushing out of which by Sephadex-saline also give satisfactory renal and bladder scans. c) Other potent therapeutic radionuclides could be retained for some time by this method, which can be in the lungs easily flushed out within 2 hours.

A simplified method for the local blood flow determination by means of $^{86}Rb$ was developed in rats and rabbits. $^{86}Rb$ in the form of chloride mixed with physiological saline was intravenously injected. The doses were $10{\mu}Ci$ for rats and $100{\mu}Ci$ for rabbits, which were injected in less than 5 seconds. The rats were sacrificed after 30 seconds, and the rabbits at the intervals of 10, 20, 40 and 60 seconds, by decapitation or rapid intravenous injection of 3 to 5ml of saturated KCI. After bleeding, the organ and tissue samples, e.g. lungs, renal cortex, jejunum and skeletal muscle were quickly removed. The $^{86}Rb$ uptake in 1 gram of the organs and tissues were measured. On the basis of uptake value, administered dose and body weight, the local blood flow was calculated. Following were the results: 1. The uptake values of $^{86}Rb$ in the above organs and tissues of rats were different from other previous reports, in which the large rats were used. It appears, therefore, that the correction on the basis of body weight is necessary. 2. The uptakes of $^{86}Rb$ in the above organs and tissues of rabbits remained rather stationary within 20 to 40 seconds. 3. The local blood flow in the above organs and tissues were calculated from $^{86}Rb$ uptake in per cent dose per 1 gram tissue for 200 gram body weight. The formula could be applied not only to the rabbits but to the rats. 4. The present method could be applied to the comparison of the local blood flow between the various organs and tissues of the control and experimental animals.