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Biomedical subjects

G Ohta

Publications and source records attributed to G Ohta.

At least 91 records · Page 5Linked to original sources
PubMed1983

Immunoregulatory T cell function in patients with primary biliary cirrhosis.

Both concanavalin A (Con A)-induced suppressor cell activity and autologous mixed lymphocyte reaction (AMLR) were significantly decreased in patients with primary biliary cirrhosis (PBC) in comparison with those of healthy subjects (p less than 0.001) and p less than 0.001, respectively). Factors inhibiting lymphocyte transformation by Con A and PHA were demonstrated in sera from a majority of the patients with PBC. In approximately half of these patients, some serum factor(s) also induced a decrease of Con A-induced suppressor cell function of lymphocytes from healthy subjects. These results suggest that patients with PBC have impaired immunoregulatory lymphocyte function which may be related to some factor(s) present in serum.

Adult↗
PubMed1982

Ultrastructural changes of bile duct epithelium in primary biliary cirrhosis in relation to progression of bile duct loss.

Using wedge liver biopsies from patients with primary biliary cirrhosis (PBC), ultrastructural features of the intrahepatic bile ducts in livers with slight or no bile duct loss were compared with those in livers with advanced bile duct loss and in extrahepatic cholestasis (EHC). Most changes in the biliary epithelium in PBC were similar to those in EHC. Microvillous loss and bleb formation, mitochondrial damage and increase in endoplasmic reticulum and ribosomes were found in PBC irrespective of the degree of bile duct loss, and also in EHC. These changes were present almost equally at any level of the biliary tree, and are presumed to represent a variety of non-specific lesions of biliary epithelial cells. As the loss of bile ducts in PBC progressed, cytoskeletal filaments and cytophagosomes increased in number and basement membranes were more thickened and reduplicated. These changes were more or less conspicuous in smaller branches of the biliary tree, and were also prominent in EHC. They might be causally related to the bile flow disturbance in the liver. Lateral intercellular spaces were irregularly dilated and contained osmiophilic membranous and/or granular material, similar to that found in duct lumena, within and without the basement membrane, and in the cytoplasm of periductal macrophages. Furthermore, pinocytotic vesicles were increased in the biliary cytoplasm facing periphery. These findings suggest possible alteration of the permeability of biliary epithelial cells, probably in the direction from the lumena to the periductal tissue. Such changes were found in PBC livers with virtual absence of bile duct loss, and the significance of this phenomenon is discussed.

Bile Ducts, Intrahepatic↗
PubMed1982

Pale eosinophilic inclusions simulating ground-glass appearance of cells of hepatocellular carcinoma.

Pale eosinophilic inclusions simulating ground-glass appearance were observed in cells of hepatocellular carcinoma. They were round or elliptical in shape, and their size was about 14 micrometers in diameter. Light eosinophilia and fine granulation with homogeneous appearance were delineated from other cellular materials. They were negative for HBsAg, blood plasma proteins including alpha 1-antitrypsin, and alpha-fetoprotein by immunohistochemical stainings. Ultrastructurally, they were well-demarcated and consisted of homogeneous finely granular matrix. Histological, histochemical and ultrastructural features were different from several intracellular inclusions hitherto reported on hepatocellular carcinoma. These changes may represent a deposition of secretory proteinous materials in cells of hepatocellular carcinoma, but their chemical and antigenetical content could not be identified.

Antigens↗
PubMed1982

Nodular hyperplasia with a central telangiectatic fibrosis in the liver of non-cirrhotic portal fibrosis (idiopathic portal hypertension).

Unusual nodules of hyperplastic hepatocytes were found in the liver of a 64-year-old woman with non-cirrhotic portal fibrosis (idiopathic portal hypertension). These nodules were subdivided by stellate fibrous tissues which, in the center of the nodules, contained conspicuous telangiectatic lesions with congestion. The latter was consisted of markedly dilated sinusoids and fibrosis of their walls either in a lack of hepatocytes or with severly atrophic hepatic column. The lesions were different from already described focal nodular lesions in the liver. No drugs and chemicals could be identified as the causative agents. The small arterial changes, namely, hyalinization and thickening of their walls and luminal narrowing or occlusion, were found in the nodular lesions and also in the remaining hepatic tissues, and might be a causative factor for the nodular lesions.

Endothelium↗
PubMed1982

Cytoplasmic blood plasma inclusions in human hepatocytes.

Hepatocellular blood plasma inclusions were demonstrated in conventional formalin-fixed paraffin-embedded liver tissue by the immunoperoxidase technique in 114 out of 197 liver specimens. They were usually round or elliptical in shape, their size varying from a few microns to about 30 microns in diameter. Albumin, fibrinogen, alpha 1-antitrypsin, IgG, IgM, IgA, ceruloplasmin and transferrin were demonstrated in the inclusions, in that order of frequency. A majority were negative with the periodic acid Schiff stain after amylase digestion, but a few were positive. Many of them seemed to correspond to vacuoles in the hepatocytes but some were not seen in HE-stained sections. The inclusions were frequently seen in autopsy liver specimens, but were rare in surgical ones. Most of the inclusions might develop at an agonal stage, probably as a result of hypoxia or circulatory disturbances in the livers.

Adult↗
PubMed1982

Caroli's disease in congenital hepatic fibrosis and infantile polycystic disease.

Two of three patients with infantile polycystic disease and all three patients with congenital hepatic fibrosis revealed multiple gross cystic dilatation of the intrahepatic biliary tree, referred to as Caroli's disease. All three patients with congenital hepatic fibrosis showed recurrent cholangitis related to coexisting Caroli's disease, and two of them died of sepsis following cholangitis. There were several common morphologic findings in the intrahepatic biliary tree of macroscopic and microscopic levels in infantile polycystic disease and congenital hepatic fibrosis with Caroli's disease: 1. irregular, non-obstructive dilatation of the duct lumen; 2. bulbar protrusion of the duct wall into the lumen; and 3. bridge formation of the duct wall across the lumen. These ductal changes might be caused by a combination of uneven and disproportionate overgrowth of biliary epithelia and their supporting connective tissue. This pathogenetic mechanism might be operative along the entire intrahepatic biliary system in this disease group, and involvement of the smaller levels in early life might result in infantile polycystic disease and congenital hepatic fibrosis and simultaneous or possibly later involvement of the larger levels in Caroli's disease.

Adult↗
PubMed1982

Studies of immune functions of patients with chronic hepatitis.

Peripheral T cells from patients with chronic active hepatitis (CAH) showed a significantly decreased suppressor effect (or increased helper effect) on allogeneic B cell differentiation into Ig-producing cells (Ig-PC) (p less than 0.05). After irradiation of T cells to eliminate suppressor influences, mean spontaneous helper activity of CAH was not different from that of healthy subjects, indicating that spontaneous helper activity of CAH was normal. Concanavalin A (Con A)-induced suppressor cell activity was significantly decreased in CAH (p less than 0.01, 9 defective cases out of 18 patients). Minor defect of Con A-induced suppressor activity was also found in some patients with chronic persistent hepatitis (CPH) (2 defective cases out of 14 patients). Autologous mixed lymphocyte reaction (AMLR) was significantly decreased in patients with CAH (p less than 0.005). Spontaneous suppressor or Con A-induced suppressor activity was not different statistically between HBsAg-positive and HBsAg-negative cases. Finally, we demonstrated a presence of a serum factor(s) that can decrease Con A-induced suppressor cell function of healthy subjects in 7 of 21 patients with CAH and 2 of 14 CPH. Our results suggest that defective suppressor cell function likely attributable to serum factor(s) may reflect altered immune responses of CAH.

B-Lymphocytes↗
PubMed1982

T cell-mediated cytotoxicity against HBsAg-coated Chang cells in patients with chronic hepatitis: evidence for cytotoxicity mediated by delayed hypersensitivity T cell reaction.

T lymphocytes from 7 (21%) of 34 patients with chronic hepatitis showed positive cytotoxicity against HBsAg-coated Chang cells. This positivity was observed in HBsAg-negative patients having positive blast transformation responses to HBsAg, as well as in patients convalescing and recovered from acute B hepatitis. Levels of S-GPT in these patients were not different from those showing no cytotoxicity. T cell-mediated cytotoxicity against HBsAg-coated hepatocytes in HBsAg-negative patients thus may have no significant pathogenetic role in destruction of hepatocytes and may represent anamnestic response of sensitized T lymphocytes to HBsAg. Positive cytotoxicity against HBsAg-coated Chang cells was also found in 3 of 17 patients with HBsAg-positive chronic hepatitis. All positive cases exhibited blast transformation responses to HBsAg and low HBsAg titers in their sera. Levels of S-GPT in these patients were significantly higher than in those showing no cytotoxicity, suggesting possible presence of T cell-mediated liver cell damage in these patients. T lymphocytes from asymptomatic HBsAg carrier showed no cytotoxicity to HBsAg-coated hepatocytes and no blast transformation responses of lymphocytes to HBsAg. From the results of the parallel occurrence of T cell-mediated cytotoxicity and blast transformation responses to HBsAg, and of presence of lymphotoxin in the supernatant co-cultured HBsAg and cytotoxicity-positive lymphocytes, it seemed likely that T cell-mediated cytotoxicity in our system might be mediated by lymphokine produced by T cells as a result of delayed hypersensitivity reaction in vitro.

Cells, Cultured↗
PubMed1982

Disordered immunoregulatory functions in patients with chronic active hepatitis.

Peripheral T lymphocytes from patients with chronic active hepatitis (CAH) showed a significantly decreased suppressor cell (or increased helper cell) effect on differentiation of allogenic B cells to Ig-producing cells (Ig-PC). Spontaneous helper cell activity as measured after irradiation of T cells appeared normal, while Concanavalin A (Con A)-induced suppressor cell activity was significantly reduced. Some patients of chronic persistent hepatitis (CPH) also showed mild depression of Con A-induced suppressor cell activity. Poor suppressor cell activity in CAH was much more often seen in HBsAg negative, autoantibody positive patients than in HBsAg positive autoantibody negative ones. Autologous mixed lymphocyte reaction (AMLR) was significantly decreased in patients with CAH. Also, a serum factor(s) that decreased Con A-induced suppressor cell function of healthy subjects could be demonstrated in some patients with CAH and CPH. Our results suggest that altered immune responses observed in CAH may be due to defective suppressor cell function, partly attributable to serum factor(s).

Autoantibodies↗
PubMed1982

Histological and histometric examination of the intrahepatic portal vein branches in primary biliary cirrhosis without regenerative nodules.

Histometric examination, based on the assumption that ratios of the sizes of portal vein branches to the sizes of the accompanying hepatic arterial branches in the portal tracts are relatively constant in normal livers, indicated that in primary biliary cirrhosis without regenerative nodules, lumens of the intrahepatic portal veins were narrowed and phlebosclerosis was frequent in patients with esophageal varices. Thus, each of these lesions of the intrahepatic portal veins might be related to the development of the presinusoidal portal hypertension that occurs in primary biliary cirrhosis without regenerative nodules. However, the exact causal relationship of this portal venopathy and the development of portal hypertension remains unknown. Damage to the intrahepatic bile ducts in primary biliary cirrhosis, associated with portal and periportal inflammation, may contribute to the development of the morphological lesions of the intrahepatic portal veins. Furthermore, spongiomatous vasculatures found around the larger portal veins, but not those around the smaller veins, appear to be related to the presence of esophageal varices.

Adult↗
PubMed1981

An autopsy case of erythropoietic protoporphyria with cholestatic jaundice and hepatic failure, and a review of literature.

A 43-year-old woman with a history of photosensitivity died of hepatic failure following 3 and a half months of unexplained jaundice. The liver was black, showed mild fibrosis and conspicuous pigment deposition in the cytoplasm of the hepatocytes, Kupffer cells and portal macrophages, and within dilated lumina of bile canaliculi and of ductules. The pigment disclosed a striking birefringence and numerous slender electron-dense crystals on electron microscopy. Similar crystals were also found within the cytoplasm of the ductular epithelium. Despite absence of cirrhosis observed in almost all previously described fatal cases the diagnosis of erythropoietic liver with marked protoporphyrin deposition so far have not been described in the cases observed at autopsy.

Adult↗
PubMed1981

Activities of lymphocytes mediating antibody-dependent cell-mediated cytotoxicity in patients with chronic active hepatitis.

Antibody-dependent cell-mediated cytotoxicity (ADCC) of peripheral blood lymphocytes against sheep erythrocytes, cultured rat hepatocytes (BRL-3A) and Chang cells in the presence of specific anti-serum was evaluated in patients with chronic active hepatitis (CAH) and healthy subjects. ADCC activities against these cells were significantly decreased in patients with CAH when compared with healthy subjects. Significant correlations were observed between degrees of ADCC against BRL-3A, Chang cells and sheep erythrocytes. In patients with CAH, percentage and absolute number of E-rosette forming cells in the peripheral blood lymphocytes were decreased but Fc-receptor bearing (EA gamma) lymphocyte concentration was normal. There was no clear-cut relationship between the concentration of EA gamma-lymphocytes and the degree of ADCC. Preincubation of lymphocytes from healthy subjects with CAH sera significantly reduced ADCC against sheep erythrocytes. Furthermore, analysis of effector lymphocytes mediating ADCC (K-cell) against BRL-3A indicated that T lymphocytes bearing Fc-receptors with lower affinity for sheep erythrocytes are active in ADCC, though a population of K-cell is heterogeneous. It seems likely that decreased T cells in the peripheral blood and possibly the presence of serum factors in patients with CAH may partly participate in impairment of ADCC.

Antibody-Dependent Cell Cytotoxicity↗