Studies on turnover changes of albumin and γ-globulin in various liver diseases were conducted to elucidate the characteristics of metabolic disturbances in these proteins and the relation to the nature of hepatic legions. In addition, the significance of the gastrointestinal metabolism of albumin on the development of hypoalbuminemia in liver cirrhosis as an extrahepatic factor was also studied.
Characteristics of turnover changes of albumin in liver diseases are the depletion of albumin synthesis or degradation, and a decreased exchangeable albumin pool (both of extravascular and intravascular albumin pools). A net transfer of intravascular albumin into extravascular compartment tended to be decreased, indicating a compensating mechanism to maintain the constant level of serum albumin. These abnormalities were correlated to the severity rather than the activity of hepatic legions.
Abnormalities of turnover changes of γ-globulin were the changes associated with the increase of γ-globulin synthesis or degradation. These changes were related to the activity of hepatic legions. A net transfer of intravascular γ-globulin into extravascular compartment tended to be increased indicating a compensating mechanism to the maintainance of the serum γ-globulin level.
No correlation between the changes of albumin and γ-globulin turnover was observed, suggesting that the changes in both proteins respectively reflected the characteristically different legions occuring in the liver.
The net excretion of albumin into the intestine in patients with cirrhosis was not greater than that in normal subjects. However, the serum loss into the gastrointestinal tract and the ratios of gastrointestinal degradation to total degradation rate of albumin were significantly higher in liver cirrhosis than in normal subjects, and there is a positive correlation between the protein loss into the intestine and the elevation of portal pressure. These results suggested that cirrhosis of the liver had a character of relative protein-losing gastroenteropathy.

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For the purpose to study the hepatic lymph flow 11% Patent Blue V was injected into the liver under peritoneoscopy and the subsequent peritoneoscopic examinations revealed the following:
1) The direction of the lymph flow on the surface of the right liver lobe can be divided into the ascending and the descending ones by the line (to be described below) as the demarcation line. This demarcation line starts from the right upper part of the liver and passes about 5cm above the liver marigin where the gall-bladder is attached to the liver, and then it runs diagonally towards the median lower direction. The lymph vessels on the liver surface situated left upper side of this line are those that run towards the diaphragm and the others that run towards Lig. falciforme hepatis. After those lymph vessels run into Lig. falciforme hepatis, they take two ways that run throgh Lig, falciforme hepatis in the direction of diaphragm and that run towards the liver hilus. Those lymph vessels located on the right under side of this demarcation line and on the posterior surface of the liver run towards the liver hilus.
2) It was proved by the dye injecting method that the lymph vessels on the liver surface were communicated with those situated in the deep portion of the liver.
The lymph vessels on the liver surface and those on the gall-bladder surface are communicated with one another at the junction of the gall-bladder and the liver.
3) When 0.3ml of 11% Patent Blue V is injected into the liver at the depth of about 5mm from the surface, the dye oozed again on the liver surface as patterns of dense, coarse, scattered or linear form.
4) In comparing the patterns of the dye appearance by this method with the peritoneoscopic findings, the patterns of scattered or linear form were characteristic of the large white liver with old scar, the patched liver, the early nodular liver, or the nodular liver. In com paring the patterns of the dye appearance with histological findings, the scattered and linear were correlated with fibrosis or the cell infiltration of Glisson's capsule and also hepatic lobular disorder.
5) In those cases showing disturbances in hepatic hemodynamics the dye appears like-weise scattered or in the linear form.

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Silica Gel of 100-200 meshes was injected into the portal vein of dogs and the peripheral end of the portal vein was blocked to bring about disturbances in the portal blood flow. After this, the changes in the hepatic lymph flow and others were observed over a long period of time. In additions, the hepatic vein of other group of dogs was ligated, and the manner of lymph flow of the liver in such ligated dogs was observed. The results may be summarized as follows.
1) Observations were carried on the serial sections (20 μ in thickness) prepared with the liver of dogs given injection of Silica Gel powder into the portal vein. As a result 10 to 20 minutes after the Silica Gel injection there were observed the portal veins blocked with Silica Gel and the other without any such blockade. The construction of liver lobules at this stage was normal. In observing the liver of such dogs with lapse of time no liver cirrhosis developed within the period of 19 months, but there were seen shunt between portal veins and fibrosis and septum formation along the direction of the potal vein. However, there could be detected hardly any round cell infiltration in the parenchyma and the mesenchyma of the liver.
2) The portal blood pressure began to rise immediately after the Silica Gel injection, which recovered to normal level several months later, but it rose again with lapse of over 12 months.
3) On observing the livers of dogs after the injection of 11% Patent Blue V into the liver, in the liver of normal dogs the dye appeared densely on the liver surface, but with the liver of the test dogs 10 to 20 minutes after the Silica Gel injection as well as several months afterwards the dye appeared on the liver surface in the scattered form aside from the dense and coarse forms Further with lapse of over one year after the Silica Gel injection, dye appeared on the liver surface as well as on the surface of gall bladder in the linear form in addition to the manners of the appearance noted above.
4) In the case where the same dye was injected into the liver of those dogs whose hepatic veins had been ligated, the dye was found to have migrated into the lymph ducts of the gall bladder in every case.

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Gastric emptying and secretion were studied by means of test meal method on healthy controls and patients with petic ulcer. The following studies were made by giving water-, caffeine-, or peptontest meal containing phenol red to the subjects, and withdrawing gastric contents after 20 minutes period. Volume of secretion and acid output were calculeted following to Hunt's formula (1951).
The results were briefly summerized as follows:
1) Good correlation was found between the maximal acid response by gastric tube method and the acid output obtained by test meal method, when 6ug/kg of penta gastrin was used as stimulant.
2) The rate of the emptying and the secretion was proved to be paralled with the volume of test meal, so far as 50ml, 200ml and 500ml of water-test meal were used.
3) Both gastric emptying and secretion were stimulated significantly by addition of caffeine to water test meal. Moreover, the similar accelerating effect of caffeine upon the gastric function was observed both in previous oral and parenteral administration. Caffeine was proved to affect upon gastric function not only by its local stimulation but also though systemic effect after absorption.
4) Pepton-test meal (2.6%) promoted acid secretion more remarkably than caffeine test meal, but no influence was observed on emptying. Acid outupt obtained by 200ml of pepton test meal in 20minutes period corresponded to 80% of that by maximal histalog stimulation.
5) Function of the stomach of patients with peptic ulcer was examined using 200ml of pepton test meal in 20minutes period.
High acid output and rapid emptying were detected in duodenal ulcer patients, and low acid output but normal emptying were observed in gastric ulcer patients.
The ratio of the acid output obtained by test meal method to maximal histalog response was about 90% in patients with duodenal ulcer, and about 80% in patients with gastric ulcer and normal controls. It was suggested that antral release of gastrin might be more active in cases with duodenal ulcer than in cases with gastric ulcer and in healthy controls.
6) Effect of some anticholinergic drugs were examined by test meal method. Propantheline bromide and total alkaloid of the scopolia root were proved to depress both gastric emptying and secretion. However, oral administration of hyoscine butylbromide affected little upon them.

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The purpose of this study is to reevaluate ¹³¹I-triolein test.
1) Basic experiments
Ten commercial ¹³¹I-triolein products were analyzed with thin layer chromatography by Stahle's method. Radioactivity of each fraction was found as follows; 10.9±6.8% in PL, 10.6±7.3% in Ch, 20.3±11.4% in FFA, 57.5±12.9% in TG and 0.7±1.0% in ChE fraction. From above results, commercial products appeared to be impure. Only triglyceride fraction of commercial ¹³¹I-triolein developed by above mentioned methods was extracted and named purified (radioiodinated) triolein.
2) Animal experiments
25 adult male dogs were fasted overnight and cannules were placed in thoracic duct, portal vein and femoral vein of dogs. Radioiodinated triolein (commercial or purified) mixed with cold meal of peanut oil was administered into the stomach or duodenum. Absorption tests without thoracic duct fistula, or with administration of ¹⁴C-triolein were performed as control. In the case of commercial triolein, the radioactivity appeared in portal blood as well as thoracic duct lymph. In the case of purified triolein administration, however, radioactivity appeared only in thoracic duct lymph and γ-ray of portal blood was negligible. So was in the case of ¹⁴C-triolein absorption tests. When thoracic duct lymph treated by 10% TCA solutions, precipitated radioactivity ratio was 90.4±6.3% in commercial triolein and 97.4±3.9% in purified triolein. By TLC method, radioactivity of thoracic duct lymph lipids existed 76.7±8.1% in the fraction of TG in commercial triolein and 86.8±3.9% in purified. In portal plasma lipids, 40% of radioactivity was found in PL fraction in the case of commercial triolein, but no γ-ray was found in all fraction in the purified triolein tests. This results means the same biochemical mechanism of absorption of purified ¹³¹I-triolein with ¹⁴C-triolein. When chylomicron composed of ¹³¹I-triolein transported into systemic blood circulation, chylomicron was metabolized and large amounts of isolated inorganic ¹³¹I appeared in blood.
3) Clinical investigations
75 commercial and 35 purified radioiodinated triolein tests were performed on hospitalized patients. Fecal excretion rate using purified ¹³¹I-triolein corresponded more to that of chemical fat balance study than the results obtained by use of commercial ¹³¹I-triolein. Only from 30 to 50% of radioactivity of the venous blood was precipitated by TCA in both cases of commercial and purified triolein administration. Radioactivity of lipids in the plasma extracted after Folch's method was evaluated in each fraction by TLC. Much radioactivity in the plasma existed in the fraction of FFA instead of TG which contained high radioactivity ratio in thoracic duct lymph. From above findings, it is not proper to speculate fecal excretion rate of ¹³¹I-triolein on the basis of radioactivity levels of blood, which are effected by the metabolism of lipids as well as absorption.

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The patient (57 years old, male) was admitted to the hospital with chief complaint of dysphagia. X-ray fluoroscopy revealed that he had carcinoma of lower esophagus of about 11cm long. The primary tumor of esophagus was irradiated by exposing of 300R per day to ⁶⁰Co before operation. When total quantity of irradiation reached 3900R, his complaint was almost disappeared and the size of the primary tumor silhouette in the X-ray film became extremely small.
When the schedule of irradiation to the primary tumor was almost finished, the patient suddenly had mortor disturbance of the left side of the body. Neurological examination revealed the patient might have a cerebral lesion at antero-temporal area which might be caused by metastatic tumor.
The neurological symtoms were completely disappeared by surgical removal of the metastatic tumor from the cerebrum. On 30 days after craniotomy, the primary tumor of the lower esophagus was resected by means of right side thoracotomy. The end of the resected esophagus was anastomosed with stomach in the thorax. Histological finding of both tumors of cerebrum and esophagus was"adenocarcinoma tubulare".
Any paper reporting that cerebral tumor metastasized from esophagus or stomach was surgically resected can not be found in Japan. In most of cases with carcinoma of esophagus or stomach, lymphnode and/or organs being close to the primary tumor might be so strongly affected by metastasis that the physical condition of the patients with cerebral metastasis could not be kept good enough for craniotomy.

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