We have measured serum group I pepsinogen (PG I) levels in the subjects with endoscopically normal mucosa and the patients with peptic ulcer in order to investigate the normal range of serum PG I levels. Serum PG I levels in the patients with recurrent ulcer and the mechanism of release of PG I into the blood stream were also studied. Mean (±S.E.) serum PG I levels in 136 subjects with endoscopically normal mucosa was 61±2ng/ml and the normal range was considered to be 30-109ng/ml from the frequency distribution. Mean serum PG I levels in the patients with recurrent gastric ulcer was not significantly higher than the value in the patients with non-recurrent ulcer. On the contrary, mean serum PG I levels in the patients with recurrent duodenal ulcer was significantly higher than the value in the patients with non-recurrent duodenal ulcer. Administration of atropine caused a significant diminution of serum PG I in the patients with duodenal ulcer, which suggests the vagal control of PG I release.
Although it has been widely accepted that the nuclear DNA content increases in human malignancies, there is a lack of evidence for sequential change of the nuclear DNA content. The present study was undertaken to investigate the nuclear DNA content in relation to the histopathological appearance by means of Feulgen-DNA-cytofluorometry in the rat of MNNG-system. The results indicate that the nuclear DNA content shows bimodal change, i.e., early increase which appeared in the phase of no detectable histological abnormality from at 2 weeks after MNNG-ingestion and late increase just before the recognition of malignancy histopathologically.
The relationships between serum pepsinogen levels (group I pepsinogens; PG I, group II pepsinogens; PG II, total serum pespinogen; T-PG) and gastric acid-pepsin outputs (BAO, MAO, PAO, BPO, SPO, PPO) have been studied in 57 patients. The correlations between PG I, T-PG and gastric acid-pepsin outputs were all statistically significant (p<0.001), particularly, there were a high correlation coefficient (r=0.84-0.87) between serum PG I, T-PG and stimulated gastric acid-pepsin outputs (MAO, PAO, SPO, and PPO). Serum PG II, also, showed the positive correlation with the acid-pepsin outputs (r=0.32-0.67, p<0.005-0.001), but less correlated than the serum PG I and T-PG. The results indicate that a high significant relationship exists between the serum pepsinogen levels (PG I, T-PG) and the stimulated gastric acid-pepsin outputs, and it was suggested that the possibility of the serological examination of the gastric analyses.
Tapeworm pernicious anemia is not so rare in the northern Europe. In Japan, no cases of tapeworm pernicious anemia have been reported, though cases of Diphyllobothriasis latum have been increasing recently. 11 cases of Diphyllobothriasis latum were given 0.25μg of 57Co-vitamin B12-human gastric juice (0.5μCi), and 0.25μg of 58Co-vitamin B12 (0.8μCi) through a Bilbao-Dotter tube inserted into the upper jejunum to know the vitamin B12 kinetics. One hour later, a flushing dose of 1mg non-labelled vitamin B12 was injected intramuscularly. The 24 hours urine was collected (Schilling test) to count 57Co and 58Co. 48 hours after the start of treatment, the modified method of Damaso de Rivas (Kihara) was performed to expell the worm, and the radioactivity (57Co, 58Co) of the worm was counted to evaluate the uptake rate of vitamin B12 by the worm. The results of Schilling test were as follows. 57Co-vitamin B12-human gastric juice: 14.1±8.1% (x±SD), 5.8-25.3% (range), 58Co-vitamin B12: 20.9±10.2% (3.0-31.9%). Abnormal values under 10% were found in only two cases each. The uptake rate of vitamin B12 by the worm varied considerably among 11 cases, e.g. 57Co-vitamin B12-human gastric juice: 8.6±8.4% (1.6-24.9%), 58Co-vitamine B12: 11.8 ± 15.5% (1.0-50.4%). It is suggested that because these VB12 uptake rates by the tapeworm are so samll, Japanese patients with Diphyllobothriasis latum tend not to develop tapeworm pernicious anemia.
Using nonoclonal antibodies, OKT series, Con A induced suppressor activity was investigated. The subsets of peripheral blood lymphocytes were evaluated by means of the method of immunofluorosecence with monoclonal antibidies in healthy subjects and patients with chronic hepatitis. Con A induced suppressor activity was observed not only in unfractionated lymphocytes but in OKT4 subset (-) fraction and OKT8 subset (-) fraction. These findings were compared between healthy subjects and patients with chronic hepatitis, but no statistically significant difference was found. After the induction of suppressor cells by Con A, using peripheral blood lymphocytes of healthy subjects, OKIal (-) subset showed increased suppressor activity as compared with OKIal (+) subset. In patients with CAH, no difference of the percentages of OKT3+ Tcell and OKT4+ Tcell was obtained, however the percentages of OKT8+ Tcell were significantly decreased and the ratios of OKT4+ Tcell and OKT8+ Tcell, OKT4/OKT8, were elavated compared to healthy subjects. From these results, it could be concluded as follows: (1) suppressor cells induced by Con A have no Ia-antigen on their cell membrane, (2) the decreased percentages of suppressor cells may be involved in the pathogenesis in patients with CAH.
The correlation between serum and liver tissue γ-glutamyl transpeptidase activities as determined by microassay method, was studied in needle biopsy samples taken from 41 patients with alcoholic liver disease, 104 patients with viral liver disease, 28 patients with drug-induced liver injury and 10 normal liver histology. Each of the mean activities of serum and liver tissue γ-GTP activities in patients with alocholic liver disease, and drug-induced liver injury was statistically higher than those of normal liver histology, respectively. The mean activities of serum and liver tissue γ-GTP in patients with alcoholic liver disease and cytotoxic drug-induced hepatitis were higher than those of viral liver disease, respectively. The mean activity of liver tissue γ-GTP in patients with cholestatic drug-induced liver injury was higher than that of cytotoxic liver injury. The frequencies of the grades of the γ-GTP activities of liver tissue taken from the patients with various liver diseases were statistically different in each of the grades of the changes of eosinophilic degeneration, necrosis and hydropic swelling of liver cells.
We have unexpectedly observed low γ-glutamyltranspeptidase (γ-GTP) activities in cases of acute intrahepatic cholestasis. In these patients, γ-GTP activity was very low in spite of a marked increase in serum bilirubin concentration and alkaline phosphatase (ALP) activity. In contrast, γ-GTP activity was increased in cases of extrahepatic cholestasis concomitant with an elevation of serum bilirubin and ALP levels. These findings suggest that low γ-GTP activity is useful in the differentiation of acute intrahepatic cholestasis from extrahepatic cholestasis. No inhibitors of γ-GTP were detected in sera of patients with acute intrahepatic cholestasis.
Plasma F-XIII activities and the localization in biopsied liver specimens were investigated in 85 patients with various liver diseases. Plasma F-XIII activities tended to be lower in accordance with the severity of hepatic parencymal damage, however they were remarkablly elevated in patients with alcoholic hepatic fibrosis. The localization of F-XIII in liver biopsy specimens of 45 cases was determined by the method of PAP. Fibroblasts, macrophages and immature collagen fiber in extensive fibrous lesions stained positively for F-XIII. XIIIa positive cells were prominent especially in cases of alcoholic fibrosis and also in cases of chronic hepatitis active. Those cases in whome many XIIIa positive cells were observed the elevation of plasma F-XIII activity. In 34 patients with chronic liver disease, the number of XIIIa positive cells also correlated with plasma F-XIII activity. These findings suggest that F-XIII may contribute to active hepatic fibrogenesis and that determination of plasma F-XIII activity and staining for F-XIIIa in the biopsied liver specimens may be useful parameter to detect the development of hepatic fibrosis.
The role of the gastric and intestinal phases with regards to pancreatic blood flow were observed by the heated thermocouple method using conscious dogs in which a tiny atraumatic element had been implanted in the pancreas. Pancreatic blood flow was observed during intragastric or intraduodenal instillation and gastric or duodenal dilatation in these dogs. Analogous pancreatic blood flow increments were observed after intragastric instillation of 5% meat soup, 1M glysine and normal saline. A pancreatic blood flow increment was also observed by mechanical gastric dilatation and the duration of this response coincided with that of gastric dilatation. A pancreatic blood flow increment occured after intraduodenal HCl instillation. Duodenal dilatation also induced a pancreatc blood flow increment. From these observations, it is supposed that the pancreatic blood flow was mainly regulated by a neural mechanism (the gastropancreatic reflex) from the stomach and by neural as well as hormonal (secretin) mechanism from the duodenum in the conscious state.
Thirty lesions of heterotopic pancreas of the stomach, that were found in 29 patients, were reviewed from clinicopathologic view point. The heterotopic pancreas as divided into two macroscopic types, α and β, which were different from each other in their location, size, mainly affected layer in the gastric wall, and constituents of the lesion. Acinic element of the pancreas was found in the lamina propria mucosae in 40% of the cases, indicating the possibility of successful endoscopic biopsies. Central concavities of the lesion were found in 57%, showing considerable variations in their configurations, of which one should be aware in diagnostic roentgenography and endoscopy.