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T Terada

Publications and source records attributed to T Terada.

At least 19 recordsLinked to original sources

Cell proliferative activity in adenomatous hyperplasia of the liver and small hepatocellular carcinoma. An immunohistochemical study demonstrating proliferating cell nuclear antigen.

BACKGROUND: Recently, adenomatous hyperplasia (AH) of the liver, a sizable parenchymal nodule in the cirrhotic liver, has been considered a preneoplastic lesion in human hepatocarcinogenesis. METHODS: The authors evaluated cell proliferative activity by immunostaining for proliferating cell nuclear antigen (PCNA) in AH (n = 30), small hepatocellular carcinoma (HCC) (n = 14), and their surrounding regenerative nodules (SRN). RESULTS: AH was categorized histologically as ordinary or atypical. Ordinary AH (n = 8) had no hepatocellular atypia, whereas atypical AH (n = 22) was composed of atypical hepatocytes that were equivocal as to benignity and malignancy. Three atypical AH contained overt malignant foci. The PCNA labeling index of ordinary AH was lower than that of SRN and the index of atypical AH was higher than that of SRN except in two cases. The PCNA labeling index of malignant foci within atypical AH was higher than that of nonmalignant areas of atypical AH and was similar to that of small HCC. For small HCC, the PCNA labeling index was much higher than that of SRN and correlated with small HCC grades. CONCLUSIONS: These data suggest that ordinary AH is a largely developed regenerative nodule with little proliferative activity and that it is not a preneoplastic lesion; the data also indicate that atypical AH has much proliferative activity, from which malignant foci with greater proliferative activity emerge. Atypical AH with or without malignant foci may represent an early stage of multi-step hepatocarcinogenesis in humans.

Aged

Cystic dilatation of peribiliary glands in livers with adult polycystic disease and livers with solitary nonparasitic cysts: an autopsy study.

Cystic dilatation of peribiliary glands of intrahepatic and extrahepatic bile ducts was investigated in autopsied livers with adult polycystic disease (n = 8), in autopsied livers with solitary nonparasitic cysts (n = 18) and in normal autopsied livers (n = 23). In normal livers, cystic dilatation of intrahepatic peribiliary glands was absent or slight, when present. In livers with solitary nonparasitic cysts, cystic dilatation of intrahepatic peribiliary glands was present in varying degrees. In livers with adult polycystic disease, intrahepatic peribiliary glands showed frequent and severe cystic dilatation so marked that it was grossly recognizable. In contrast, peribiliary glands of the extrahepatic bile ducts showed no cystic dilatation in most cases, regardless of the three conditions examined. Liver parenchymal cysts were numerous in livers with adult polycystic disease, few in livers with solitary nonparasitic cysts and nonexistent in normal livers. Von Meyenburg complexes were present in 87.5% of livers with adult polycystic disease, in 16.7% of livers with solitary nonparasitic cysts and in 4.3% of normal livers. These findings suggest that intrahepatic peribiliary glands undergo cystic dilatation in livers with adult polycystic disease-and, to a lesser degree and frequency in livers with solitary nonparasitic cysts, probably because of congenital or genetic factors-and that these cystic changes may comprise a part of numerous cysts of adult polycystic disease.

Adult

MRI changes in embolized meningiomas.

Study of the MRI changes that occur after superselective embolization of hypervascular meningiomas with Gelfoam powder (5 cases) and polyvinyl alcohol (PVA) particles 150-250 microns in size (4 cases) has indicated that, after embolization, meningiomas showed loss of the signal void, decrease in gadolinium-DTPA contrast enhancement, and prolonged T1 and T2. Shortening of T1 and T2 was seen in two patients with Gelfoam-embolized meningiomas in whom CT showed pooling of iodinated contrast medium in the tissue. In vitro experimental data demonstrated that the shortening of T1 and T2 was due to the iodinated contrast medium.

Aged

A method for quantitative measurement of cerebral vascular permeability using X-ray CT and iodinated contrast medium.

Cerebral vascular permeability is an important consideration in treatment for intracranial tumours. We have developed a new method to measure the cerebral vascular permeability quantitatively using a conventional X-ray CT scanner and iodinated contrast medium. We have already applied our method in 50 cases of intracranial tumour and 5 cases, which establish the methodology, are demonstrated. Dynamic CT scanning of a section including the tumour and the superior sagittal sinus was performed over 40 min after bolus injection of contrast medium, and 25 images were acquired. Our theoretical model of contrast enhancement was applied to analyse time-density curves, and the following parameters were obtained: Ki (inward flux constant), Kb (backward flux constant), Vp (vascular plasma volume), and lambda (extracellular fluid space volume). Furthermore, functional maps were generated from parameters for each pixel. Changes in intra-arterial iodine concentration, required in our model, were measured from CT numbers in the superior sagittal sinus. We have investigated several aspects of our method. Histological findings in surgical specimens of intracranial tumours agreed well with the parameters obtained by our method. Vp was verified quantitatively by single photon emission computed tomography. Our method was shown to be reproducible. These results show that the parameters are useful for assessing tumours and in planning chemotherapy. Our method, which employs no special equipment, is readily available at any institution.

Adult

Local blood flow changes in malignant brain tumours under induced hypertension.

Changes in tumour blood flow under an induced hypertensive state were examined in malignant brain tumours to know if the precondition for the effectiveness of induced hypertensive chemotherapy--relative increase in tumour blood flow--are fulfilled. Tumour blood flow was measured under both a resting and an induced hypertensive state in 12 patients with various malignant brain tumours (6 gliomas, 6 metastatic brain tumours) using xenon-enhanced computed tomography. The blood pressure was elevated 40% above the systemic blood pressure of the resting state by the infusion of angiotensin II. Tumour blood flow increased 30% on average above the normal brain tissue blood flow after the induction of an induced hypertensive state (p < 0.05). The tumour blood flow increased in 11 cases of malignant tumours, but decreased in one case with massive brain oedema after induced hypertension. The increase in blood flow was higher in hypervascular tumours and less in hypovascular tumours. Therefore, induced hypertensive chemotherapy probably will be more effective in hypervascular malignant brain tumours with small mass effects.

Adult

Cell kinetic analyses and expression of carcinoembryonic antigen, carbohydrate antigen 19-9 and DU-PAN-2 in hyperplastic, pre-neoplastic and neoplastic lesions of intrahepatic bile ducts in livers with hepatoliths.

We evaluated cell proliferative activity and expression of carcinoembryonic antigen (CEA), carbohydrate antigen 19-9 (CA 19-9) and DU-PAN-2 in various bile duct lesions in livers with hepatoliths, using histochemical and immunohistochemical methods. Histologically, the bile duct lesions were divisible into hyperplasia, dysplasia, adenocarcinoma in situ and invasive adenocarcinoma. All cases showed mucosal hyperplasia in stone-bearing bile ducts. Livers with invasive adenocarcinoma frequently contained adenocarcinoma in situ and dysplasia, and livers with adenocarcinoma in situ occasionally harboured dysplasia. Proliferating cell nuclear antigen (PCNA) labelling index was low in hyperplasia (mean +/- SD = 20.5 +/- 8.7%), intermediate in dysplasia (35.4 +/- 15.9%), and high in adenocarcinoma in situ (46.4 +/- 9.3%). The mean number of argyrophilic nucleolar organizer regions (AgNORs) was low in hyperplasia (1.52), intermediate in dysplasia (2.26) and high in adenocarcinoma in situ (2.69). There was a significant positive correlation between PCNA labelling index and AgNORs count. CEA was expressed on invasive adenocarcinoma cells and adenocarcinoma in situ cells in most cases and on dysplastic cells in about a half, while CEA was never present in hyperplastic epithelia. Expression of CA 19-9 was low in adenocarcinoma, intermediate in dysplasia and rather high in hyperplasia. There was no significant difference in DU-PAN-2 expression among these bile duct lesions. These data suggest that cell replicative activity is low in hyperplasia, intermediate in dysplasia and high in adenocarcinoma in situ, and that CEA appears in the following order: dysplasia, adenocarcinoma in situ, invasive adenocarcinoma. We suggest that carcinogenesis in biliary epithelial in livers with stones is a multi-step process through hyperplasia, dysplasia and adenocarcinoma in situ to invasive adenocarcinoma.

Adenocarcinoma

Hamartomatous lesion of the liver in an adult patient with biliary dilatations: a variant of inflammatory pseudotumor of the liver?

An unusual tumor-like lesion (1.2 cm in diameter) in the left lobe of the liver in a 67-year-old woman with dilatations of the common and hepatic bile ducts is reported. Histologically, this lesion was composed of hyalinized connective tissue, several dilated bile ducts with periductal fibrosis and biliary epithelial proliferation, lymphocytic and plasmacytic infiltrates, stenotic venous and arterial vasculature, and nerve bundles. Although these elements were found in a disordered pattern and appeared to have a hamartomatous etiology, each of these pathologic components seemed inflammatory in character. Besides, clinical data disclosed that this lesion was acquired in origin. Although such a hepatic tumor-like lesions has not previously been reported to the best of our knowledge, this tumorous lesion shared features of hepatobiliary lesions reported in intrahepatic calculi, a form of chronic cholangitis. It seems likely that this tumor-like lesion might have arisen from localized chronic cholangitis, possibly related to the dilatations of the common and hepatic ducts, and we suggest that this lesion be named "fibroductal variant" of inflammatory pseudotumor of the liver.

Aged

Argyrophilic nucleolar organizer region counts in exocrine pancreatic tumors.

We enumerated the number of Ag-NORs in normal pancreatic ducts and exocrine pancreatic tumors to assess their cellular activity. Our results indicate that the mean number of Ag-NOR counts increased stepwise in the following order: normal pancreatic duct (1.26), serous cystadenoma (1.27), mucinous cystadenoma (1.65), mucinous cystadenocarcinoma (2.29), noninvasive intraductal variant of mucin-producing papillary adenocarcinoma (3.16), and a common type of invasive duct cell adenocarcinoma (3.78). These results suggest that cellular proliferative activity is low in normal pancreatic ducts and serous cystadenoma, intermediate in mucinous cystadenoma, and high in mucinous cystadenocarcinoma and duct cell adenocarcinoma. In addition, mucinous cystadenocarcinoma has significantly lower Ag-NOR counts than duct cell adenocarcinoma. We conclude that a clear quantitative difference between the Ag-NOR content of tumor cells of serous cystadenoma, mucinous cystadenoma, mucinous cystadenocarcinoma, and duct cell adenocarcinoma reflects the underlying different biologic behavior (chiefly, grade of malignancy) of these lesions.

Carcinoma, Intraductal, Noninfiltrating

Characterization of bovine liver cytosolic 3 alpha-hydroxysteroid dehydrogenase and its aldo-keto reductase activity.

1. 3 alpha-Hydroxysteroid dehydrogenase was purified to homogeneity from bovine cytosolic fraction, which was monomeric and its molecular weight was estimated to be about 35 kDa. 2. The enzyme had ability to catalyze NADP(H)-dependent oxidoreduction of position 3 alpha-hydroxy and keto group of steroids and also could catalyze the reduction of some ketones and quinones. 3. In addition, benzenedihydrodiol was one of the substrates of dehydrogenase activity with NADP+. 4. Indomethacin, synthetic steroids and SH-reagents were potent inhibitors for this enzyme. 5. Inactivation of the enzyme by GSSG-treatment was restored to its original activity by the addition of DTT. 6. The presence of coenzyme, 0.33 mM NADP+, completely protected from the DTNB-inactivation. 7. Bovine liver cytosolic enzyme immunologically crossreacted with rat liver 3 alpha-hydroxysteroid dehydrogenase.

3-Hydroxysteroid Dehydrogenases

Purification and characterization of glutathione S-transferase isozymes in dog lens.

1. Two isozymes of glutathione S-transferase (GST-dl1 and GST-dl2) were purified to homogeneity from dog lens. 2. The subunit size and the isoelectric point were determined to be 24,000 and > pI 9.5 for GST-dl1 and 22,000 and pI 8.1 for GST-dl2. 3. It was judged that GST-dl1 is a class alpha enzyme and GST-dl2 belongs to class pi on the basis of their immunological properties and N-terminal amino acid sequences. 4. The expression pattern of glutathione S-transferase isoenzymes in dog lens is different from that in pig, rat and bovine lenses.

Amino Acid Sequence

Pathologic observations of intrahepatic peribiliary glands in 1,000 consecutive autopsy livers: IV. Hyperplasia of intramural and extramural glands.

Hyperplastic changes of intrahepatic peribiliary glands have rarely been reported, with the exception of hepatolithiasis. To determine whether there are any hyperplastic changes in the glands in livers without hepatolithiasis, we examined 1,000 consecutive autopsy liver specimens that had no hepatolithiasis. The glands were divided into intramural mucous glands and extramural seromucous glands. The hyperplastic changes were found in "normal" livers and in livers with various hepatobiliary diseases, and they were classified into three categories: hyperplasia of intramural glands (49 cases; 4.9%), hyperplasia of extramural serous acini (35 cases; 3.5%), and hyperplasia of extramural mucous acini (92 cases; 9.2%). Two or more of these three hyperplastic changes occasionally coexisted in the same liver. Hyperplasia of intramural glands was seen rather evenly in normal livers and in livers with various hepatobiliary diseases. Prevalence of hyperplasia of extramural serous acini was high in intrahepatic cholangitis and submassive hepatic necrosis. Prevalence of hyperplasia of extramural mucous acini was high in cirrhosis, submassive hepatic necrosis, cholangitis, systemic infection, and extrahepatic biliary obstruction. The hyperplastic intramural glands and mucous acini of extramural glands contained more neutral, carboxylated, and sulfated mucin than normal glands. Although their pathogenesis is unclear, these hyperplastic changes may enhance seromucous secretion into biliary lumens and may lead to biliary dysfunctions such as retardation of bile flow and increased bile viscosity. These hyperplastic changes may be preexisting conditions predisposing to hepatolithiasis.

Autopsy

Vascular supply in adenomatous hyperplasia of the liver and hepatocellular carcinoma: a morphometric study.

Vascular supply of adenomatous hyperplasia (AH) of the liver, a preneoplastic or early neoplastic lesion of hepatocellular carcinoma (HCC), and that of HCC were morphometrically examined. Seventy-three nodules of AH were divided into 43 ordinary and 30 atypical AHs. The latter showed a variety of hepatocellular atypias that were, however, insufficient to make a diagnosis of HCC, while the former lacked such atypias. Arteries were slightly more numerous and portal veins were slightly less frequent in both ordinary and atypical AHs compared with the surrounding liver. In ordinary AHs, cumulative areas of arterial lumen and portovenous lumen were almost equal to or less than those in the surrounding liver in two thirds of our cases. The cumulative area of arterial lumen was equal to, and that of portovenous lumen was less than, the cumulative area in the surrounding liver in the remaining one third of our cases. In a majority of atypical AHs, the cumulative area of arterial lumen was equal to, and that of portovenous lumen was less than, the cumulative area in the surrounding liver. In most HCC nodules, the number and cumulative luminal area of arteries were much more, and those of portal veins were much less, than the number and cumulative area in the surrounding liver. The relative number and cumulative luminal area of abnormal arteries compared with all arteries showed a stepwise increase in the following order: ordinary AH (20.7% and 17.5%), atypical AH (46.8% and 52.5%), and HCC (93.6% and 92.0%). These data suggest that ordinary AH, atypical AH, and HCC are different in vascular supply, and that these differences may reflect sequential changes in the hemodynamic state during hepatocarcinogenesis.

Aged

Study on human erythrocyte thioltransferase: comparative characterization with bovine enzyme and its physiological role under oxidative stress.

Thioltransferase, an enzyme which catalyzes the thiol/disulfide exchange reaction in the presence of GSH, was purified to homogeneity on 15% SDS-PAGE from human (36,000-fold purification) and bovine (23,000-fold) erythrocyte hemolysates. These enzymes had similar properties in their monomeric structures (M(r) = 11,000) and broad specificities for substrates ranging from low-molecular disulfides (S-sulfocysteine, cystamine, and cystine) to protein disulfides (trypsin and insulin). They were highly sensitive to SH-reagents (monoiodoacetic acid and mercuric chloride), but were protected from inactivation by the presence of disulfides (GSSG, cystamine, and cystine). Phosphofructokinase and pyruvate kinase that had been inactivated by disulfides were reactivated effectively by the addition of thioltransferase with GSH. In addition, disulfides in membrane proteins of human erythrocytes that have been oxidatively damaged by diamide treatment were reduced to the SH-free form more effectively by incubation with thioltransferase.

Amino Acids

A novel dihydrodiol dehydrogenase in bovine liver cytosol: purification and characterization of multiple forms of dihydrodiol dehydrogenase.

Three enzymes (DD1, DD2, and DD3) having dihydrodiol dehydrogenase activity were purified to homogeneity from bovine cytosol. DD1 and DD2 were identified as 3 alpha-hydroxysteroid dehydrogenase and high-Km aldehyde reductase, respectively, as judged from their molecular weights, substrate specificities and inhibitor sensitivities. DD3 was a unique enzyme which could specifically catalyze the dehydrogenation of trans-benzenedihydrodiol and trans-naphthalenedihydrodiol without any activity toward the other tested alcohols, aldehydes, ketones, and quinones. The Km value of DD3 (0.18 mM) for benzenedihydrodiol was lower than those of other dihydrodiol dehydrogenases so far reported. DD3 immunologically crossreacted with DD1, but showed no crossreactivity with DD2. Additionally, DD3 was inhibited in a competitive manner, with a low Ki value of 1 microM, by androsterone, which was a good substrate for DD1. It was assumed that DD3 is a novel enzyme which is specific to dihydrodiols, exhibiting similarity to DD1 in immunological and structural properties.

3-Hydroxysteroid Dehydrogenases

Histological features and interphase nucleolar organizer regions in hyperplastic, dysplastic and neoplastic epithelium of intrahepatic bile ducts in hepatolithiasis.

Neoplastic transformation occurs in the intrahepatic biliary tree in hepatolithiasis. The present study aimed to clarify the neoplastic processes by correlating the histological features of the bile duct lesions with counts of interphase argyrophilic nucleolar organizer regions (AgNORs), which reflect cell proliferative activity. We studied 55 cases of hepatolithiasis and 25 normal autopsy livers. The biliary epithelial lesions in hepatolithiasis were divisible into hyperplasia, dysplasia and neoplasia. These lesions were found in bile ducts containing calculi. All cases of hepatolithiasis showed a varied degree of hyperplasia. Additionally, eight cases showed dysplasia, five non-invasive intraductal adenocarcinoma and 10 invasive adenocarcinoma. Cases of non-invasive and invasive carcinoma frequently harboured areas of dysplasia, and areas of dysplasia and non-invasive carcinoma, respectively. The mean and standard deviation of the number of interphase AgNORs in the normal and abnormal biliary epithelium showed a step-wise increase in the following order: normal (1.32 +/- 0.36), hyperplasia (1.52 +/- 0.37), dysplasia (2.28 +/- 0.56), non-invasive carcinoma (3.23 +/- 1.00), and invasive carcinoma (3.72 +/- 0.77). These histological and cell kinetic observations suggest that, in hepatolithiasis, carcinogenesis in bile duct epithelial cells progresses in a multi-step manner, through hyperplasia, dysplasia, non-invasive adenocarcinoma and invasive adenocarcinoma.

Adenoma, Bile Duct

Immunohistochemical study of carcinoembryonic antigen in mucinous cystic neoplasm of the pancreas.

Pathologic and immunohistochemical studies of 13 patients with mucinous cystic neoplasm of the pancreas were performed in order to determine whether these lesions represent overt or latent malignancy. In 9 patients with mucinous cystadenoma, the foci of mucus-rich columnar epithelia formed the usual pattern of stratifications and papillary projections with a benign appearance and did not stain with mouse monoclonal antibody to CEA (CM-010, Mochida, Japan). In contrast, the foci of mucus-poor columnar epithelia which were in a focal distribution showed moderate to severe atypical hyperplasia and reacted strongly with anti-CEA in 6 of the 9 patients. In addition, areas of both noninvasive and invasive mucinous cystadenocarcinomas in 4 patients, which were composed primarily of mucus-poor columnar epithelia, showed diffuse cytoplasmic and/or apical reactivity with anti-CEA. Based on these results, we conclude that severe atypical epithelial hyperplasia composed primarily of mucus-poor columnar epithelia represents a precursor to mucinous cystadenocarcinoma, and, therefore, mucus-poor atypical epithelia may undergo malignant transformation.

Adult

Characterization of multiple forms of carbonyl reductase from chicken liver.

Three enzyme forms (CR1, CR2 and CR3) of carbonyl reductase were purified from chicken liver with using 4-benzoylpyridine as a substrate. CR1 was a dimeric enzyme composed of two identical 25-kD subunits. CR2 and CR3 were monomeric enzymes whose molecular weights were both 32 kD. CR1 exhibited 17 beta-hydroxysteroid dehydrogenase activity as well as carbonyl reductase activity in the presence of both NADP(H) and NAD(H). CR2 and CR3 had similar properties with regard to substrate specificity and inhibitor sensitivity. They could exhibit the activity only with NADPH and had no hydroxysteroid dehydrogenase activity. CR2 and CR3 cross-reacted with anti-chicken kidney carbonyl reductase antibody, though CR1 did not. The results suggest that CR1 is a hydroxysteroid dehydrogenase, and CR2 and CR3 are similar to each other and to the kidney enzymes.

17-Hydroxysteroid Dehydrogenases

Immunohistochemical and immunoelectron microscopic analyses of alpha-amylase isozymes in human intrahepatic biliary epithelium and hepatocytes.

The expression and localization of the pancreatic and salivary isozymes of alpha-amylase in the intrahepatic biliary epithelium and hepatocytes were examined by the immunohistochemical method with polyclonal and monoclonal antibodies in 45 normal autopsied human livers. Immunoelectron microscopic studies with the protein A-gold method were performed with the monoclonal antibodies (MAb) on seven of the livers. The intrahepatic biliary system was divided into large ducts, septal ducts, interlobular ducts, bile ductules, and peribiliary glands. Immunohistochemically, pancreatic isozyme was observed in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, and peribiliary glands in almost all livers. Interlobular ducts expressed pancreatic isozyme in only four (9%) livers. Bile ductules and hepatocytes were negative for pancreatic isozyme in all cases. Expression of salivary isozyme was observed in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, interlobular ducts, bile ductules, and peribiliary glands in almost all livers, although the expression in interlobular ducts and bile ductules was weak. Hepatocytes were weakly positive for salivary isozyme. Immunoelectron microscopy revealed that both pancreatic and salivary isozymes were located in the supranuclear cytoplasm of the epithelium of large ducts, septal ducts, and peribiliary glands, and that hepatocytes had no pancreatic isozyme but contained salivary isozyme. These data suggest that pancreatic and salivary isozymes of alpha-amylase are produced by the intrahepatic biliary epithelium and secreted into intrahepatic biliary lumens, and that they may play an important role in the physiology of the intrahepatic biliary tree and hepatic bile. It is also suggested that hepatocytes produce a small amount of salivary alpha-amylase that may be secreted into the biliary tree.

Antibodies, Monoclonal