Helicobacter pylori (Hp) is considered to be one of the causes of gastric mucosal injury. Using biopsy specimens from the gastric mucosa of patients with gastritis or gastric ulcer, the intramucosal mucus was quantified by computer image analysis to evaluate its relationship with Hp. In gastric mucosa positive for Hp, the mucus content within the gastric mucosa was significantly decreased. Ammonia was administered based on its assumed role in decreasing the mucus content of the gastric mucosa, and resulted in a decrease in rats to whom it was administered. Based on these results, cases of intractable gastric ulcer were studied. In these intractable cases, Hp was present significantly more often than in other cases and the intramucosal mucus content was significantly lower. These findings suggest that Hp may be a factor in the resistance of gastric ulcer to treatment.
It is known that cysteamine-induced duodenal ulcers in rats are similar to the human duodenal ulcers in some aspects. We investigated their similarities in view of adrenalin-stimulated gastric acid secretion and gastrin secretion in these rats. Acid outputs decreased in the control group by the administration of adrenaline, but in the cysteamine-administrated group acid outputs increased dosedependently. Serum gastrin levels and plasma noradrenalin levels increased by cysteamine administration. The abnormal gastric acid secretion by the adrenalin infusion in the process of cysteamine-induced duodenal ulcers in rats, which was resembled to that of duodenal ulcer patients, was recognized.
A human colon cancer cell line Caco-2 undergoes spontaneous enterocytic differentiation under the standard culture condition. We examined the changes in the proliferative activity of Caco-2 cells during the differentiation, and the effect of serum factors on this spontaneous differentiation. Caco-2 cells cultured in FCS-containing media exhibited the differentiation phenotypes such as dome formation and increase of ALP activity after the 6th day of culture. Cell cycle analysis showed a marked decrease in S phase cell population during the cell differentiation. When Caco-2 cells were cultured in FCS free media, the cell population of S phaseremained unchanged during culture period and the differentiation phemotypes were not induced. The addition of FCS to Caco-2 cell cultured in the absence of FCS resulted in the rapid induction of the differentiation phenotypes. These results suggest that differentiation of Caco-2 cells is closely related to the reduction of cell proliferation and requires some factors in FCS.
Serum concentration of angiotensin-converting enzyme (ACE) were measured in 34 patients with Crohn's disease. ACE was decreased in Crohn's disease compared with healthy controls. Significant negative regression between ACE and CDAI was observed. It suggested intestinal ACE may play a regulatory role in intestinal inflammation of Crohn's disease. Among the patients, ACE did not show the significant change by use of prednisolone nor by location of disease. The mechanism of ACE decrease in Crohn's disease was not known, but this phenomena may be one of the reason of persistant inflammation of Crohn's disease.
Mapping specimens of 6 cases of ulcerative colitis included adenocarcinoma invaded into submucosa (invasive carcinoma) were made and immunohistochemical quantitative analysis of ras p21, an oncogene product and secretory component were examined in invasive carcinoma, severe and moderate dysplasia of ulcerative colitis. Large intestinal carcinoma invaded into submucosa, colonic adenoma and normal mucosa were examined as the control. Index values of Staining Density (ISD) and of Staining Gland (ISG) of ras p21 demonstrated significantly higher values in invasive carcinoma, severe and moderate dysplasia of ulcerative colitis than adenoma (P<0.01). ISG of secretory component in moderate dysplasia and adenoma showed significantly high value compared with severe dysplasia and invasive carcinoma of ulcerative colitis (P<0.05). The collective evidence indicates that severe dysplasia falls into the same category with invasive carcinoma of ulcerative colitis and may be defined as carcinoma in situ. Moderate dysplasia was also defined as carcinoma in situ or borderline lesion.
Optimality in branching structure of the hepatic arterial vessel in 16 patients with liver cirrhosis was studied. The controls used in this study were 14 patients with gastric or colonic cancer not accompanied by liver dysfunction. Optimality principle was based on the concept that blood vessel size and arrangement provided for blood flow with minimum energy loss. Measurements were made of parent and branch vessel diameters from selective celiac arteriogram. After that we measured the included angles of the branchpoints of portal vein using ultrasonography. The branchpoints of interest were the third bifurcations of right intrahepatic portal vein and artery. The following results are presented in terms of three parameters (r22/r12, r1/r0, and r2/r0). The theoretical equations have been shown by several authors. The curve representing these equations was shown by Zamir. We analyzed the scatter of the data points and compare the theoretical and actual results with them. The extent of the scatter is studied making a comparison between control patients and patients with cirrhosis. The data points in control patients were plotted near the theoretical curve. In patients with cirrhosis, the data points show a definite tendency to be plotted far away from the theoretical curve, when we take account of both vessel diameters and branching angles. This discrepancy between theoretical values and actual data in patients with cirrhosis is considered to be caused by the following factors which may influence the vascular structure; hemodynamic change caused by increase of intrahepatic shunt, and morphological change caused by increased fibrosis or/and parenchymal nodules of the liver.
Technetium-99m galactosyl human serum albumin (TcGSA) is a synthesized radiolabeled analog ligand to asialoglycoprotein receptor, which resides only at a mammalian hepatocyte. TcGSA studies were performed on 16 patients with various acute liver disease and 3 controls with normal livers. Dynamic data were obtained by a gamma camera during 35 minutes after an intravenous injection of 3mg (185MBq) of TcGSA. The parameters of TcGSA timeactivity curves were obtained by dividing radioactivity of the liver by that of the liver plus heart at 15min (Receptor Index), and by dividing radioactivity of the liver at 15min by that at 3min post injection (Clearance Index). The two parameters correlated well with prothrombin time, clinically estimated staging, and severity of acute liver disease. We have concluded that liver function study by the newly developed receptor imaging with TcGSA can be a sensitive and promising tool in estimating the severity and prognosis of acute liver disease.
Nineteen cases (male 6, female 13) of acute obstructive suppurative cholangitis (AOSC) were divided into 2 groups and were studied, Group A; over 70yrs old (12), Group B; under 70yrs old (7). The most frequent etiology of AOSC was choledocholithiasis (Group A 75%, Group B 43%). Urgent biliary drainage was performed in 18 cases, and which were clinically improved. The decreasing rate of bilirubin were fair in both groups and only 2 cases in Group A were dead. Concerning with the laboratory findings on admission, Group A had a higher level of BUN than Group B, and there were no other significant differences. Complications were frequently occurred in Group A (Shock 83%, DIC 83%, Renal failure 42%). The diameter of choledochus at biliary drainage was below 9mm in 45% of cases in Group A, which implied the rapid progression to AOSC from the onset of biliary obstruction. Early diagnosis and urgent biliary drainage were essential for the management of AOSC in the old age.
To investigate the pathogenesis of hereditary pancreatitis we determined whether pancreatic stone protein (PSP) gene was structually altered in two independent families diagnosed as hereditary pancreatitis. Because, it has been shown that a decrease in the activity of PSP which inhibits CaCO3 crystal formation in pancreatic juice is closely related to the development of chronic calcifying pancreatitis. Southern blot analysis revealed neither a rearrangement nor a gross deletion of PSP gene in genomic DNA of affected members of both families. Furthermore, six exons of PSP gene amplified by polymerase chain reaction from genomic DNA was directly sequenced, while no apparent base mutation was observed. The immunohistochemical study utilizing monoclonal antibody to PSP showed the presence of immunoreactive PSP in the section of pancreatic tissue obtained from a patient affected with hereditary pancreatitis. However, the level of immunoreactive PSP in the remaining acinar cells of the patient pancreas was not reduced when compared with that of normal pancreas. Results, therefore, indicate that genetic alteration of PSP gene may not be responsible for the pathogenesis of hereditary pancreatitis.