By means of cholecystography and examination of duodenal juice, the function of the gallbladder was investigated on 25 inpatients with tuberculosis in respiratory organs (chiefly in lungs) who had dyspeptic complaints.
The following results were obtained;
1) Patinets with more than 30 cc of gall in the gallbladder totaled 14 of 20 (70%).
2) 65% of patients (in 13 of 20) were found to be under normal level in Meulengracht unit of B-bile.
3) 52% of patients (in 13 of 25) had deformed gallblders.
4) Those patients whose shadows of gallbladders on X-ray film were smaller than those of average in square measure came to 44% in 11 of 25.
5) Patients with such gallbladder that did not contract normally on chlecystography totaled 16 of 25 (64%).
Dyspeptic symptomes and signs disappeared a few days after giving choleretica (orally or by injection).
In considerating of our cases, it is our viewpoint on cholecystopathy involved in the tuberculosis in the respiratory organ that gastrointestinal disorders due to the tubercle bacillus and its toxin are not responsible, but biliary dyskinesia caused by them might be primarily responsible for dyspeptic complaints.

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Electoron microscopic investigations were carried out in the experimental dogs with pancreatic impairment, with reference to the ultrastructure and morphological chages in the columnar epithelium cells of upper jejunum after administration of olive oil and oleic acid.
1. In the observation of the columnar epithelium cells of normal dogs, lipids were generally appeared to be hydrolyzed in the lumen of the intestine and absorbed into the columnar epithelium cells in mechanism undetectable with the electoron microscopy.
Then in the cells, they were supposedly resythesized removing through the endoplasmic reticulum and the Golgi complex. Mitochondria and small particulate componet suggested to play a role in the resynthesis of the lipids. Subsequently, the lipids were consolidated in the membrane system of perinuclear portion, stored in the Golgi complex, and finally extruded into the lateral intercellular space.
2. The dogs with acute pancreatitis were produced by infusion of olive oil into the main pancreatic duct. On the 4 th day after the operation, the columnar epithelium cells revealed abnormalities in the mitochondria and the endoplasmic reticulum, as well as reduction of the small particulate component. In this condition, disturbed absorption of both olive oil and oleic acid were observed.
The evidence suggests that pancreatic impairment causes the abnormality of the columnar epithelium cells, which is led disturbed absorption of lipids.
3. On the 4 th week after the operation, there were minimal or no changes either in the ultrastructure or in the absorptive function of the columnar epithelium cells.
The evidence suggests that the changes of the columnar epithelium cells induced by pancreatitis is reversible.
4. In the columnar epithelium cells of the dogs on the 7 th day after the pancreatectomy, there was observed significant reduction of the endoplasmic reticulum and the small particulate component. And in this condition, no absorption of olive oil and oleic acid were observed, even though administered with pancreatic digestive drugs.
In this case, generally disturbed metabolism of the individuals seems to cause the destruction of the columnar epithelium cells and provoke imrpaired lipid absorption.

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Though splenomegaly is one of the common manifestations in portal hypertension, the pathogenesis in the developement of splenomegaly remains unclear. An attention was forcused to investigate the intrasplenic pressure as an index of intrasplenic circulation, and the histological characteristics of the spleen.
Since 1960, Prof. Imanaga has proposed a classification of portal hypertension according to the state of intrahepatic circulation as follows;
Group I Extrahepatic obstruction of the portal vein
Group II Intrahepatic obstruction of the portal vein
Group III Intrahepatic obstruction of
1) hepatic vein
2) hepatic and portal veins
Group IV Extrahepatic obstruction of the hepatic vein
An observation was carried out on 77 cases including 10 normal and 67 enlarged spleens who belonged to Group II and Group 111-2 but some cases.
The spleen biopsies, measurement of portal and intrasplenic pressure were examined and the findinge were compared with the state of intrasplenic circulation.
The results obtained were as follows;
1) The intrasplenic pressure was always higher than the portal pressure but one exception. In almost all cases the intrasplenic pressure was proportional to the elevated portal preure; i) the intrasplenic pressure elevated with an average of 383mmH₂O, the portal pressure also elavated with an average of 350mmH₂O in 30 cases of Group II, ii) the intrasplenic pressure elevated with an average of 404mmH₂O, the portal pressure also elevated with an average of 372mmH₂O in 30 cases of Group 111-2.
2) Elevated portal preseure was reduced to the normal level and the enlarged spleen decreased in size after end-to-side portacaval anastomosis. In such cases the intrasplenic pressure was also reduced remarkably; i) the intrasplenic pressure was depressed to an average of 214mmH₂O in 19 cases of Group II, and ii) in 16 cases of Group 111-2 the pressure also was depressed to an average of 219mmH₂O.
3) Histological characteristics of the spleen with portal hypertension were divided into two types; “reticulofibrosis” and “fibroreticulosis”. In Group II the reticulofibrosistype was found in 67 per cent of the patients, whereas in Group III-2 with cirrhosis the fibroreticulosistype was noticed in 73 per cent of the patients.
However, since there were many indifinite types of these histological alterations in both group, any definite pathogenesis in the development of splenomegaly was not demonstrated on the ground of these histological findings, as to whe ther the enlarged spleen be as primary or secondary.
4) The histological findings, i. e. the grade of fibrosis and sinushyperplasia, were considerably correlated with the grade of elavated intrasplenic pressure.
In conclusion, the results obtained led us to suggest that elevated portal pressure due to intrahepatic obstruction of the portal vein may primarily play a role in the development of splenomegaly.

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A progress has been made on the study of chronic gastritis by means of gastrocamera in Japan. It has been noted, however that gastrocamera findings are not necessarily in accord with histological findings.
To make diagnosis more acculate through gastrocamera, author has studied on some factors assured to cause such incompatibility.
1. Adherent mucus, i. e. one of characteristic features of gastrocamera finding on superficial gastritis, and swallowed saliva and airbubbles are often confused on the clinical observation. Preadministration of 2 ml. of di-methylpolisiloxan drops was successful to make saliva and air-bubbles diaapear through the while.
From the fact that no adherent mucus was found on fresh excised stomach specimens in this study, it proves inconclusive sign in gastrocamera diagnosis of superficial gastritis.
2. When 20mg. of Buscopan Complex was intravenously preadministered to the patients previously diagnosed as “spastic stomach” through gastrocamera, figure of atrophic gastritis was observed among some patients, while normal figure of gastric mucous membrane was found in other patients.
It was established, accordingly, that diagnosis of atrophic gastritis would be influenced by degrees of elongation of stomach-wall.
3. Hypertrophic gastritis diagnosed through gastroscopic and/or gastrocamera examination is not necessary conform to findings through histological examination. Then author names the former as “endoscopic hypertrophoid change”, in order to distinguish from the latter.
Before the gastrocamera examination, 20 to 40 mg. of Buscopan Complex was preaddministered te the patients, previously diagnosed as “endoscopic hypertrophoid change”. The result was that figure of atrophic gastritis was observed among some patients, while normal figure was also found others. None of “endoscopic hypertrophoid change” was observed on excised stomach specimens of the patients.
It is assumed that “endoscopic hypertrophoid change” is composed confusedly of the hypertonic state of smoothmuscles in T. muscularis mucosa and T. muscularis propria of the stomach, and of the rugged figure on hyperplastic gastritis.

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A study was conducted concerning arginine metabolism in liver damage. Arginine, glycocyamine, arginase, creatine, creatinine and GOT in serum was measured to the purpose. Results were as follows.
1. Each amount of arginine and glycocyamine in rabbit serum indicated the minimum value 1-2 days after poisoning by CCl₄, while arginase indicated contrarily an evident increase at that time. Creatine increased slightly. However, its relation with glycocyamine, a prodromal substance of creatine, could not be clarified.
2. For the recovery from the decrease of arginine at the time of poisoning by CCl₄, injection of glucuronic acid, prednisolone soluble, orotic acid or aspartic acid was seen to be efficacious. Also, administration of 10% L-arginine-L-glutamate was seen to induced an increase of serum arginase and a continuous decrease of serum arginine with relation to the former.
3. Serum arginine and glycocyamine in patients with hepatic disease were within normal range, except some decreasing cases in part of them with severe liver damage. Serum arginase increased slightly or a little more in patients with liver disease. The amount of serum arginine in patients with acute hepatitis seemed to have a negative relationship with the activity of serum arginase and serum GOT. That amount of serum arginine was unchanged in most of the patients with liver dIsease, was assumed to be due to the fact that increase of serum arginase activity was not so remarkable. The serum creatine in the patients with liver disease revealed no abnormality.

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