At present, the effect of anti ulcer drugs is evaluated simply by calculating the cumulative healing rate at a certain period of the treatment, which does not implicate any analysis of healing speed. Here, a new method of statistical analysis of ulcer healing speed is hypothetically introduced. A non-linear regression analysis is performed between two variables t (period of observation) and y (non-healing rate), obtaining an exponential function y=Ae-kt. Practically, the equation is, y=100: 0_??_t<Ti, y=100e-k(t-Ti): Ti_??_t. The theoretical values obtained from the equation are very much close to the observed values. The regression parameters are defined as follows; k: healing rate constant, Ti: initiation time of clinical healing, T1/2: half-life of non-healing rate, T50: time of 50% healing. With this method, the effect of drugs on ulcer healing is dynamically analyzed, being expressed by digital parameters with regard to healing speed.
In our clinical experiences, immune response against K.O. extract was demonstrated in a patient with acute hemorrhagic colitis associated with K.O. by leukocyte migration inhibition test. To determine the immunological mechanism implicated in the pathogenesis of K.O. associated colitis in man, we compared the incidence of experimental colitis in mice treated with intraperitoneal injection of AB-penicillin and inoculation of K.O. in cecum among the various immune states. In the group of immune suppressive ICR-mice irradiated by X-ray, the incidence of induced colitis (29%) was significantly lower than that (64%) in the non-irradiated controls. In the group of normal BALB/c-mice, hyperimmune mice immunized with K.O., mice receiving whole splenic cells from K.O. immunized syngeneic mice, mice receiving T-cells from K.O. immunized syngeneic mice, and mice receiving non-T cells from K.O. immunized syngeneic mice, the incidence of induced colitis were 45%, 75%, 71%, 75% and 11%, respectively. These findings suggest that cell mediated immunity to K.O. plays an important role in the pathogenesis of acute hemorrhagic colitis associated with K.O.
Histological examination for ova of schistosoma japonicum was performed in surgical specimens of laparotomy during 20 months from Oct., 1983 to May, 1985, in the 1st Department of Surgery, Yamanashi Medical College. Calcified schistosomal ova were detected in 54 cases out of 282, and its ratio, 19.1%, was higher than that of previous reports in Japan, including Yamanashi Prefecture. Organ distribution of ova was observed as follows; high incidences in liver (22.5% in all cases), duodenum (22.7%), colon and rectum (18.8%), and stomach (17.2%). No ova were detected in bile tract (108 cases), spleen (31 cases), and esophagus (31 cases). Among these 54 cases of chronic schistomomiasis japonica, 22 cases of liver fibrosis and 5 cases of liver cirrhosis in which 3 cases accompanied hepatocellular carcinoma. It suggests an epidemiological relationship between schistosomiasis japonica and hepatocellular carcinoma. According to Japan Autopsy Annual in Yamanashi Prefecture for 10 years (1973-1982), schistosomiasis japonica was accompanied in 20.5% of patients.
In this study, the mechanism of hyperdynamic systemic circulation in cirrhotic patients was studied. Ninety one cirrhotics were deviled into two groups, (A) and (B), according to results of KICG; in group A, K is above 0.09min-1 and in group B, K is below 0.09min-1. Systemic hemodynamics were studied by inserting a Swan-Ganz catheter and plasma volume, intraoperative portal vein pressure, plasma catecholamine concentration, and plasma glucagon concentration were measured in each patient. In group B patients the hyperdynamic systemic circulation was more marked than in group A; the more severe the liver damage is, the higher hyperdynamic state was observed. This hyperdynamic change seems to depend mainly on an increase of plasma volume, which significantly correlates with increase of peripheral a-v shunt and increase of portal vein pressure. Plasma catecholamine and glucagon also seems to aggravate the hyperdynamic systemic circulation.
The following conlusions were acquired after experimental study of the efficacy of cimetidine, 16, 16-dmPGE2, and vagotomy for hepatic regeneration in the prevention of stress ulcers after hepatectomy. (1) The onset of water stress ulcers was noticeably lessened in all three groups. (2) The number of cases of endocytosis after hepatectomy of 3H-thymidine decreased dramatically in the vagotomy group. The rate also decreased in the cimetidine and the 16, 16-dmPGE2 groups. The decreases were evident for thymidine kinase activity and the amount of DNA for all three groups. (3) The peak value in the mitotic indedx of the vagotomy group decreased, and the rate of hepatic regeneration was noticeably lower. We concluded from these three facts that the vagotomy operation is an inadequate treatment method for preventing stress ulcers after hepatectomy.
A hypoglycemia is one of the manifestations of paraneoplastic syndrome seen in hepatocellular carcinoma (HCC). Studies were made on seventeen cases of HCC with hypoglycemia, concerning the pathogenetic mechanism of the hypoglycemia associated with HCC. A hypoglycemia was observed in 2.9% of all HCC cases. It occured usually as a terminal sign of the patients with HCC. HCC with hypoglycemia generally showd to have a rapid growing giant tumor, rapid elevation of AFP and frequent association of other signs of paraneoplastic syndrome. Most of these cases were associated with liver cirrhosis and had a slow decrease of fasting blood glucose in he clinical course, and were demanded a large amount of glucose administration to be corrected. They showed no characteristic liver pathology for hypoglycemia and so did pancreatic histology. The glucose tolerance test revealed a flat curve, low responce of IRI and c-peptide, and high level of fasting glucagon. Therefore insulin, insulin-like avtivity and glucagon were considered to have less primarily contribution to the pathogenesis of hypoglycemia. It was consequently concluded that a hypoglycemia with HCC was mainly caused by excess glucose conssumption because of rapid growing giant tumor, and by decrease of glucose production in the liver plus malnutrition because of regression of liver parenchyma of glucose metabolism in the liver due to encoachment of the tumor and the presence of the liver cirrhosis.
In 23 patients with small hepatocellular carcinoma (HCC) less than 3cm in size at the time of detection, the growth and extension of tumors and clinical findings of patients were followed for a period of 20 months on average without anticancer therapy. Speed of the tumor growth was measured in terms of doubling time (DT) from increase of tumor volume on the echogram. DT of tumors smaller than 2cm was 11.3 months on average in 10 patients, while that of tumors of 2-5cm was 6.2 months in 19 patients. The former was significantly longer than the latter. Growth speeds of HCCs of a size of 2-5cm were divided into three groups, slow growth (DT_??_6.0 Mos), intermediate growth (3_??_DT<6.0Mos) and rapid growth(DT<3.0Mos). During the natural course, the echographic pattern of the rapid and intermediate growth groups changed from the nodular type to the multinodular or massive type, and that of the slow growth group continued to be nodular in the majority. Prognosis was poorer in the rapid and intermediate groups that the slow growth group. Histologically, the tumors of the slow growth group showed Edmondsson-Steiner's grade I or II, and of a microtrabecular and monotonous pattern. The tumors of the rapid growth group showed Edmondson-Steiner's grade II and III, and of a micromacrotrabecular and mosaic pattern. One case of the rapid growth group showed Edmondson-Steiner's grade IV. There were more habitual drinkers in the slow and intermediate groups than in the rapid growth group. DT on the average in habitual alcohol drinkers was 12.8Mos and significantly longer than 6.0mos of DT in non-habitual alcohol drinkers. A tumor of a size of 3cm showing AFP level of 400ng/ml was more frequently in the rapid growth group than the others.
Morphological characteristics of the hepatic sinusoidal cells of rats, isolated by metrizamide density centrifugation and centrifugal elutriation, were studied by transmission and scanning electron microscopies (EM). The isolated Kupffer cells revealed irregular shaped nuclei and abundant lysosomes and autophasic vacuoles in the cytoplasm. Many slender and long processes on the cell surface by scanning EM were observed. Mitochondria and endoplasmic reticulum were scanty in the isolated endothelial cells. Sieve plate-like pores were seen in about 60% of the cells, but not others. On the scanning EM, short processes on the cell surface were coarsely seen. The isolated Ito cells were characterized by lipid droplets which vary in size and abundant slightly dilated rough endoplasmic reticulum. Many wavelike and undulated processes were seen by scanning EM. These results indicate that scanning EM is useful for the identification of the hepatic sinusoidal cells, as well as transmission EM.
The purpose of this study is to estimate the role of glycoprotein of pancreatic juice in alcoholic pancreatic damage. Pure pancreatic juice was obtained from 11 healthy controls and 30 alcoholics after secretin and pancreozymin injections by endoscopic retrograde catheterization of the papilla. Concentration of hexosamine, hexose and fucose, the main sugar components of glycoprotein, were measured as well as volume and concentration of bicarbonate, amylase and protein. After the collection of pure pancreatic juice, conventional ERCP was performed. ERCP findings of healthy controls were all normal (Control group). Alcoholics were classified into Normal group (n=11), MIP group (n=10) which has irregularly dilated side branches in more than one third of the pancreas, MOP group (n=5) and ADP group (n=4), according to the ERCP criteria of chronic pancreatitis established by Japanese Gastroenterological Association in 1983. Exocrine pancreatic function in MIP group was considered to be normal, but hexosamine concentration of pure pancreatic juice in this group was significantly higher than that in both Control group and Normal group. This high hexosamine concentration in MIP group is though to result from hypersecretion of mucin produced from proliferated goblet cells of irregularly dilated side branches and condensation of pancreatic juice in the pancreatic ducts and ductules. Hexosamine concentration of pure pancreatic juice increased in accordance with the severity of ERCP findings. Concentration of hexose and fucose demonstrated the similar behavior as hexosamine. It is concluded that glycoprotein of pancreatic juice plays an important role in the development of alcoholic pancreatic damage even in its early stage. Furthermore, this result suggests that the analysis of glycoprotein of pure pancreatic juice is valid for assessment of alcoholic pancreatic damage especially in its early stage.
It is well known that various enzymes of the human body increase and further more peculiar isoenzymes appear in the serum of the patients with malignant tumor. Creatine kinase isoenzymes (CK-BB) are one of the peculiar isoenzymes. Many papers have been reported on the appearance of CK-BB, cytoplasmic isoenzyme, in the serum of the patients with malignant tumor. Recently, mitochondrial CK (m-CK), which is different from cytoplasmic isoenzymes (CK-MM, CK-MB, and CK-BB) and existing in mitochondrial fraction, has been noticed because its possibility of the relation to malignant tumor. In this study, we evaluated m-CK in the serum of the patients with malignant tumor, particularly with the cancer of the gastrointestinal tract. Consequently, we found atypical CK isoenzyme in the serum of patients with malignant tumor, which is enzymatically very similar to m-CK (in the normal tissue). This atypical CK isoenzyme can be divided into at least two types according to the molecular weight. The appearance of this atypical CK suggested its specificity to the cancer.