Distribution of the silver positive cells in the mucosa of the gastritis stomach and relation between these cells and the scattered intestinal metaplasia were investigated. Materials were one hundred resected stomachs, which more or less revealed accompanied gastritis, irrespective of a main lesion : polyp, ulcer or carcinoma. In addition to HematoxylinEosin and PAS-Alcianblue double stainings, Masson-Fontana's staining was used to look for argentaffine cells and Grimelius' method for argyrophil cells. The latter method had been modified in part by the author to save a staining time. It was significant that in a considerable degree distribution of the silver positive cells in the gastritis mucosa corresponded with that of the scattered intestinal metaplasia. The silver positive cells were much frequently found around the intestinal metaplasias, particularly those scattered. However, sometimes these cells could be found even within the extension of the intestinal metaplasias. The silver positive cells were likely to extend in one direction, forming a stripe of these cells. Number of intestinal metaplasias was independent of the main lesion. As far as investigated by the silver impregnation and the fluorescence examination, the silver positive cells were proved to be argentaffine cells containing serotonine. A gland, which consists of a large number of argentaffine cells but of little Paneth's and goblet cells, without brush borders, can be named an immature intestinal metaplasia; or this can be called a pseudo-Brunner's gland, when taking account of its resemblance to a Brunner's gland. Differentiation between the immature intestinal metaplasia and the pseudo-Brunner's gland was thought to be difficult. Based on some enzymatical findings an intestinal metaplasia is classified either into a large-intestine type or a small-intestine type. The metaplasia mentioned above can be distinguished from these two types, and a new classification of the intestinal metaplasia is suggested from a histochemical point of view.

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Since the first report that argentaffin cells appeared in intestinal metaplasia of the stomach was made by Hamperl, several related studies have been performed. However many problems still remain in regard to the distribution and count of the silver positive cells in the stomach. In this paper, the distribution of the silver positive cells in the proliferative lesion and intestinal metaplasia of the stomach with hyperplastic polyp, metaplastic polyp, atypical epithelium and cancer was investigated. The order of the count of silver positive cells is as follows : in intestinal metaplasia and metaplastic polyp, in hyperplastic polyp and atypical epithelium and in gastric cancer. The silver positive cell counts in early cancer and in advanced cancer were compared showing little differences. Early cancer was divided into two types, protruded type and depressed type and advanced cancer was divided into localized type and infiltrated type. The cell counts were moderately more in depressed type and in infiltrated type than in other types. In gastric cancer, the cells were found in undifferentiated adenocarcinoma more frequently than in differentiated one. The cells have been considered as argyrophil cells and argentaffin cells. Argentaffin cells were found in the regions of intestinal metaplasia and metaplastic polyp, while both cells were seen in other proliferative lesions. The distribution and count of the silver positive cells were very similar in the regions with hyperplastic polyp and with atypical epithelium. In the author's study on the distribution and count of the silver positive cells of the stomach, atypical epitelium might be not considered as a malignant sign.

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A number of pathogenetic factors have been proposed as the etiology of chronic pancreatitis. It is also recognized in laboratory animals the pancreatic duct obstruction or the stasis of pancreatic juice produced findings similar to the human chronic pancreatitis. On the other hand, several authors have been suggested that obstruction of the main pancreatic duct caused by carcinoma of the pncreas give rice secondary to chronic pancreatitis. It is sure, therefore, that the pathological investigation of the so-called tumor concomitant pancreatitis will be also very important for the pathogenesis of the chronic pancreatitis in general. In the part I of this paper, sixty autopsy cases of primary carcinoma of the pancreas are studied histopathologically, and in the part II, the tumor concomitant pancreatitis which is located proximal (tail side) to the tumor, is studied histopathologically in comparison with the pancreatic tissue distal (head side) to the tumor. Part I : Incidence of carcinoma of the pancreas in my series of the autopsy cases is 1.3% (1.4% in male and 1.2% in female). The peak incidence is between 60 and 70 years of age in both sexes. Sites of the tumors in order of the frequency are the head (41.7 %), the tail (15.0%), the body and tail (15.0%), the head and body (10.0%), the whole (10.0%), and the body (8.3%). The histologic classification of the tumor and its incidence are as follows; ductal carcinoma (88.3%), acinar cell carcinoma (8.3%) and indeterminate origin (3.3%). The modes of the tumor extension show some relationships with primary site of the tumor; carcinoma of the head easily infiltrates to the common bile duct and duodenum, whereas the portal invasion, hematogenous and lymphogenous metastases or pleuroperitoneal dissemination are frequently occured in the carcinoma of the body and tail, and the whole. A higher incidence of hamatogenous metastases are observed in the histological type of adenoacanthoma. Generalized jaundices are observed clinically and anatomically in 63% of the subjects and it has been seen in high frequency with the carcinoma of the head or the head and body. Ascites was found in 82%. Carcinoma of the body and tail, and whole type tend to produce ascites. Carcinomatous peritonitis and tumorous portal obstruction have been considered as the main cause of the severe ascites. In this paper, histogenesis of the carcinoma of the pancreas has also been discussed. Part II : The characteristic findings which belong to the chronic pancreatitis are noted in non-tumor bearing pancreatic tissue proximal (tail side) to the tumor. These findings are observed in very high frequency and with significant differences to the distal (head side) part of the pancreas beyond the tumor. The feature has been manifested by fibrosis, pancreatic duct dilatation, epithelial changes of the pancreatic ducts elastic fiber proliferation, inflammatory cell infiltration and peripheral fatty infiltration. Changes such as acinar dilatation with proliferation of centroacinar cells, rupture of the pancreatic ducts and fatty and/or parenchymal necrosis revealed no significant differences to the distal (head side) part of the pancreas beyond the tumor. These findings could not be said as the main features for the tumor concomitant pancreatitis. However, it is considered that these findings were caused by the stasis of the pancreatic juice in the early stage of the main pancreatic duct obstruction and the incidence decreased in the late stage of the disease. The fibrotic change of pancreas is the most important conception and characteristic change for the chronic pancreatitis in view of pathology and it is also the most dominant change in the tumor concomitant pancreatitis. In most cases with intensive fibrosis, the pancreatic parenchyma almost disappear and falls into pancreatic cirrhosis with persistent and/or hypertrophic islets of Langerhans.

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