For researching the clinical significancy on mucopolysaccharide of pancreatic juice in chronic pancreatitis, the author determined hexosamine (Hxm) of duodenal juice obtained after pancreozymin and secretin stimulations. Hxm of pancreatic juice was determined in the fractions collected 20-40 minutes after secretin stimulation. The following results were obtained. Hxm of pancreatic juice increased in the group of alcoholics except pancreatitis and the chronic pancreatitis group, and particularly it was higher in the group of pancreatitis caused by alcohol than in the group of pancreatitis of other causes. Among the cases of alcoholic pancreatitis, Hxm showed remarkable increase particularly in the cases of relapsing type. Mucopolysaccharide which increased in the pancreatic juice was analyzed to find out that it was acid mucopolysaccharides except hyaluronic acid and chondroitin sulfate ABC, and perhaps it appeared to be sulfated glycoproteins. As Hxm in pancreatic juice increased in the alcoholics group and the alcoholic pancreatitis group, it was recognized intake of alcohol for a long time is an important factor for increase of mucopolysaccharide in pancreatic juice. The fact that remarkable increase of Hxm was particularly observed in the relapsing type of alcoholic pancreatitis suggests an important role of mucopolysaccharide in pancreatic juice in recurrent attacks of pancreatitis pathophysiologically, and it is an interesting finding as to formation of pancreatic calcification.
Biochemical studies on proliferation and maturation of rat fundic and jejunal epithelial cells were performed. By using frozen horizontal sectioning technique to mucosal epithelial cells of fundus and jejunum, correlation between cell proliferation and maturation were studied. The incorporation of TdR-14C into acid-insoluble fraction was measured as a marker of cell proliferation and the development of activities of specified enzymes of those tissues were assayed as markers of maturation. Studies on incorporation of TdR-14C with rat fundus revealed that radioactivity of TdR-14C was quickly incorporated into lower part of surface epithelium and mucous neck zone. Radioactivity which was incorporated into proliferative zone migrated to the top of surface epithelium about 65 hours after the injection. About 180 hours after the injection, however almost all the radioactivity shed from mucous membrane of fundus, radioactivity remained slightly on the mucous neck zone and deeper part of fundic glands. Two directions of migration of fundic epithelial cells were suggested. One was upward direction from the proliferative zone. Cells migrated up and shed from the surface epithelium during short period. The other was downward direction from the proliferative zone. Cells migrated down very slowly or stayed for a while at proliferative zone. Enzymatic studies with fundus showed that zone with the activities of specified enzymes coincided with the histological distribution of marker cells. Zone with activity of fucosyltransferase coincided with the distribution of mucous producing cells, zone with pepsinogen with chief cells and zone with Mg++-HCO-3 ATPase with parietal cells. Studies on incorporation of TdR-14C with jejunum revealed that radioactivity was quickly incorporated into crypts zone. The radioactivity migrated up along villi and shedfrom the tip of villi about 48 hours after the injection. Enzymatic studies with jejunum showed that sucrase and alkaline-phosphatase activities were low in crypts and greatly increased along the villi from crypts to tips. Studies on incorporation of TdR-14C and enzymatic studies suggested gastiointestinal cells matured during migration.
Cell regeneration is the universal repairing process of the tissue against damages. Incorporation of tritiated thymidine into the nuclei has been shown to be the most reliable indicator of this process. In the present investigation, Leevy's in vitro autoradiography technique was used to study the liver biopsy specimens of the patients with various liver diseases. Seven subjects operated for abdominal disease and one hundred three patients with various liver diseases were studied. The results were as follows: 1. In healthy livers, the number of labelled cells per 10, 000 hepatic cells was 3 for hepatic cell, 5 for Kupffer cell, but usually 0 for lymphocyte, fibrocyte and vascular endotherial cell. 2. In livers from the patients in the convalescent stage of acute hepatitis, labelling of hepatic cells increased to 3.2 times that of healthy livers. A slight increase in the number of labelled cells was observed in Kupffer cell, lymphocyte, cholangiole and fibrocyte. A causal relationship between spotty necrosis and labelled hepatic cells was not observed. 3. In livers from patients with chronic hepatitis, a marked increase in the number of labelled cells was observed in Kupffer cell, hepatic cell, lymphocyte, cholangiole, fibrocyte, epithelial cell of interlobular bile duct and vascular endotherial cell in decreasing order. Labelling into hepatic cell, cholangiole, lymphocyte and fibrocyte in the active form of chronic hepatitis was more frequent than in those of the inactive form. Labelled lymphocytes in the portal areas were mostly medium in size. 4. In livers from the patients with liver cirrhosis, labelled cells were more numerous than healthy livers, but no such difference was observed between liver cirrhosis and chronic hepatitis. In most cirrhotic cases, the number of labelled hepatic cell was less than that of acute hepatitis. The characteristic feature was the increased labelling into cholangiole and fibrocyte. This phenomenon was more apparent in the cirrhotic liver of type A' than type B. 5. In livers from the patients with subacute hepatitis, an increased number of labelled cells was observed in Kupffer cell, lymphocyte, cholangiole and fibrocyte. Labelled hepatic cells were fewer than in those of the patients in the convalescent stage of acute hepatitis.
Studies on the nucleic acid metabolism of choline-deficient rat livers were carried out using Leevy's in vitro autoradiography technique. The liver specimens were incubated for 2 hours in a culture medium containing tritiated thymidine as discribed elsewhere. The rats were fed on diets of 3 different composition: protein and fat content were same throughout the experiment; 48 percent sucrose was used as the standard choline-deficient diets, while in experimental diets, 10 or 20 percent xylitol was substituted for sucrose. The results were as follows: 1. No appreciable change in deoxyribonucleic acid metabolism was observed in rats fed on diets containing xylitol as a substitute for sucrose. 2. Substitution of 0.4 percent choline chloride was observed to prevent fat content of hepatic cells and secondarily to normalize the deoxyribonucleic acid metabolism in the rat livers. This phenomenon occurred in spite of the fact that the rats fed a low protein diet. 3. The rats fed a diet containing 10 percent xylitol tended to prevent the occurance of fatty livers and deoxyribonuleic acid metabolism of the livers was seen to be affected by fat accumlation of hepatic cells. 4. Substitution of 20 percent xylitol in the diet exhibited greater effect in preventing fat accumlation in the rat livers, but the mechanisms of the effect was seen to be independent of deoxyribonucleic acid synthesis.
Amylase isoenzymes were identified by use of agar or cellogel electrophoresis and quantified by densitometry of the zymogram in patient's sera showing hyperamylasemia following various surgical operations. In 5 out of 18 cases with radical mastectomy or orthopedic operations and in 12 out of 34 cases with operations by spinal anesthesia, hyperamylasemia was found. The increased activity of serum amylase was salivary origin in all cases above mentioned. Out of 87 cases with operated cholelithiasis, 18 cases were found to have hyperamylasemia. In 14 cases with postoperative hyperamylasemia following simple cholecystectomy, all of them were owing to amylase of salivary origin. However, hyperamylasemia owing to increased amylase of pancreatic origin was found in 4 cases following cholecystectomy plus choledochotomy or papilloplasty. In 24 out of 46 cases with gastrectomy, postoperative hyperamylasemia was seen. Hyperamylasemia due to increased activity of amylase of pancreatic origin was seen in 17 cases, and all of them had gastrectomy and lymphnode dissection (R2). In fasting sera of normal subjects, the ratio of salivary amylase to pancreatic amylase was increased when compared with that of control subjects. Furthermore, it was experimentally demonstrated that amylase activity of salivary gland of starved rats was markedly increased, although that of pancreas was decreased. From these findings, it is concluded that most of postoperative hyperamylasemia following various operations which do not give any direct damage on pancreas is owing to increased amylase activity of salivary origin, and this phenomenon might be induced by starvation.