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T Terada

Publications and source records attributed to T Terada.

At least 199 records · Page 11Linked to original sources
PubMed1996

Activation of p34(cdc2) kinase around the meiotic resumption in bovine oocytes cultured in vitro.

The p34(cdc2) kinase has been identified as a protein factor that is a regulator of meiotic maturation in mammalian oocytes. To investigate the regulatory function of the meiotic resumption in bovine oocytes cultured in vitro, the changes in the phosphorylation states of p34(cdc2) kinase and the histone H1 kinase activity were examined around germinal vesicle breakdown (GVBD). All bovine oocytes just after isolation from their follicles were arrested at the germinal vesicle (GV) stage, and these extracts exhibited two (upper and lower) bands of p34(cdc2) kinase on SDS-PAGE followed by immunoblotting with an antibody against C-terminal peptide of p34(cdc2). When these oocytes were cultured for 24 h in a medium supplemented with 100 microg/ml genistein, tyrosine phosphorylation inhibitor, GVBD was induced in 85% of oocytes, indicating that the upper band of p34(cdc2) kinase in bovine oocytes at the GV stage was already fully phosphorylated tyrosine residue prior to culture. Another (middle) band of p34(cdc2) kinase between the upper and lower bands appeared in the extracts of the oocytes cultured for 4 h, and significant activation of the histone H1 kinase was found in these oocytes (67 +/- 18 fmol/h/oocyte) as compared to that in oocytes cultured for 0 h (46 +/- 11 fmol/h/oocyte). The staining intensity of the middle band and the activity of the histone H1 kinase were further increased after the initiation of GVBD at 6 h of culture, but the quantitative changes of upper and lower bands were not detected throughout the 12 h of culture. Thus, it is concluded that the dephosphorylation of p34(cdc2) kinase followed by activation of the histone H1 kinase after the onset of culture plays a key role in the resumption of meiosis in bovine oocytes.

Journal Article↗
PubMed1996

Expression of MUC apomucins in normal pancreas and pancreatic tumours.

The epithelial expression of apomucins MUC1, MUC2, MUC3, and MUC5/6 was examined in normal pancreas and in pancreatic lesions, using immunohistochemical methods. In normal pancreas (n = 5), MUC1 apomucin was expressed in ducts and some acini, but there was no expression of MUC2, MUC3, or MUC5/6. In chronic pancreatitis (n = 5), MUC1 apomucin was expressed, but expression of the other apomucins was not noted. However, mucous hyperplastic foci of pancreatic ducts expressed MUC5/6 apomucin in 2/5 cases (40 percent). In intraductal papillary-mucinous neoplasm (IPMN) of the pancreas (n = 9), MUC1, MUC2, MUC3, and MUC5/6 apomucins were expressed in 8/9 (89 percent), 0/9 (0 per cent), 4/9 (44 per cent), and 9/9 (100 per cent) case, respectively. In pancreatic mucinous cystadenoma (n = 8), MUC1, MUC2, MUC3, and MUC5/6 apomucins were expressed in 7/8 (88 percent), 0/8 (0 percent), (25 percent), and 3/8 (38 percent) cases, respectively. In invasive ductal adenocarcinoma of the pancreas (n = 25), expression of MUC1, MUC2, MUC3, and MUC5/6 apomucins was found in 25/25 (100 percent), 1/25 (4 percent), 20/25 (80 percent), and 24/25 (96 percent) cases, respectively. Atypical mucous duct hyperplasia near cancer cells consistently expressed MUC1 apomucin and occasionally expressed MUC3 and MUC5/6. In positive cases, MUC1 apomucin expression was noted in the cell membrane facing the ductal or neoplastic lumina, while expression of MUC2, MUC3, and MUC5/6 apomucins was found in the cytoplasm. These results suggest that MUC3 and MUC5/6 apomucins newly emerge during the neoplastic transformation of pancreatic mucinous cystadenoma and IPMN and during pancreatic ductal carcinogenesis, while MUC1 apomucin remains positive and MUC2 apomucin remains almost negative during neoplastic transformation.

Aged↗
PubMed1996

The role of angiogenic factor bFGF in the development of dural AVFs.

PURPOSE: Dural arteriovenous fistulas (dAVFs) are known to be acquired disorders. Angiogenic stimulants, such as basic fibroblast growth factor (bFGF), may be involved in the evolution of this disorder. We examined the appearance and localization of bFGF, in human dAVF sinuses, versus a control using immunohistochemical techniques, to evaluate these qualitative differences. PATIENTS AND METHODS: Four human dural sinuses from dAVF patients, and one control dural sinus were removed at surgery or autopsy and used for this study. Immunohistochemistry for bFGF was performed in all five specimens to identify its appearance and localization. Immunohistochemistry for alpha smooth muscle actin, factor VII related antigen, and macrophage (CD-68) were done in all tissues to identify the bFGF positive cell types. RESULTS: In the control dural sinus, there was negative staining by bFGF immunohistochemistry. However, in all four sinuses of the dAVF patients, smooth muscle cells, endothelial cells, and meningeal cells were stained positively in various degrees by bFGF immunohistochemistry. CONCLUSION: bFGF may be significant in the development of dAVFs, judging from its strong immunoreactivity in the sinuses of dAVF patients.

Adult↗
PubMed1996

Transcortical mixed aphasia with left frontoparietal lesions.

We present a case of transcortical mixed aphasia following a left frontoparietal infarct caused by vasospasm after subarachnoid haemorrhage. Although CT showed low-density areas in the left frontal lobe and basal ganglia, single photon emission CT revealed a wider area of low perfusion over the entire left hemisphere, except for the left perisylvian speech areas. Hence, transcortical mixed aphasia may be caused by the isolation of perisylvian speech areas due to disconnection from surrounding areas.

Aphasia↗
PubMed1996

Detection of transforming growth factor-alpha protein and messenger RNA in hepatobiliary diseases by immunohistochemical and in situ hybridization techniques.

Transforming growth factor-alpha (TGF-alpha) is a cytokines related to cell proliferation and transformation. Immunoreactive TGF-alpha protein is expressed in regenerating hepatocytes and interlobular bile ducts as well as in hepatocellular carcinoma. Although TGF-alpha is thought to play an important role in the intrahepatic biliary tree, its role in cellular physiology is poorly understood. This study investigates the expression of TGF-alpha and its messenger RNA (mRNA) in various hepatobiliary diseases. The authors showed by immunohistochemistry that TGF-alpha and its receptor, epidermal growth factor receptor (EGFR), were expressed in interlobular bile ducts, proliferating bile ductules, and most hepatocytes in various hepatobiliary liver tissues. They also showed by Western blot analysis that TGF-alpha protein was present in hepatic bile samples obtained from patients with obstructive jaundice. In situ hybridization showed that TGF-alpha mRNA was localized in hepatocytes of some pathological liver tissues, but it was absent in biliary epithelial cells of the same tissues. These findings suggest that TGF-alpha protein is produced by hepatocytes, and hepatocyte stimulation occurred as autocrine growth regulation. The release of TGF-alpha into hepatic bile caused biliary proliferation and transformation through EGFR, present on the existing cell surface membrane of biliary epithelial cells.

Bile↗
PubMed1996

Preoperative embolization of meningiomas fed by ophthalmic branch arteries.

BACKGROUND: The efficacy of preoperative embolization for hypervascular meningiomas mainly fed by the branches of the ophthalmic arteries was examined. CASES AND METHODS: Five hypervascular meningiomas mainly fed by the branches of the ophthalmic arteries, four posterior ethmoidal arteries, one anterior falx artery, and one recurrent middle meningeal artery were embolized with Gel-foam powder, polyvinyl alcohol (PVA) particles, and/or microcoils as a preoperative treatment using a microcatheter. RESULTS: Catheterization of the ophthalmic and tumor feeding artery was possible and feeding arteries and lesion embolization were effective to reduce the bleeding during surgery in all cases. In three cases, visual acuity and visual field were preserved. However, in one case, visual acuity and visual field defect appeared due to the migration of Gelfoam powder (Upjohn, Kalamazoo, MI) into the retinal artery. In another case, the retinal artery was embolized with the feeding arteries since the patient was already blind. CONCLUSION: Embolization of hypervascular meningioma feeding vessels arising from the ophthalmic artery is possible and effective with preservation of vision, if embolic agents are injected gently enough not to reflux into the central retinal artery.

Adult↗
PubMed1996

Alpha-smooth muscle actin-positive stromal cells in cholangiocarcinomas, hepatocellular carcinomas and metastatic liver carcinomas.

AIMS/METHODS: In the human liver, alpha-smooth muscle actin (ASMA) is present in smooth muscle of the vasculature, perisinusoidal cells (Ito cells), and myofibroblasts derived from perisinusoidal cells. In this study, we investigated ASMA-positive stromal cells and their relation to tumor fibrosis in 50 cholangiocarcinomas, 30 hepatocellular carcinomas, and 57 metastatic liver carcinomas. RESULTS: Tumor fibrosis was much more extensive in cholangiocarcinomas and metastatic liver carcinomas than in metastatic liver carcinomas. ASMA immunoreactivity was prominent in the sinusoids surrounding cancer nodules and in the cancerous stroma, not in sinusoids remote from cancer nodules. ASMA-positive stromal cells were divisible into peritumoral ASMA-positive perisinusoidal cells and intratumoral ASMA-positive stromal cells. Both types of ASMA-positive cells were abundant in cholangiocarcinomas and metastatic liver carcinomas, but much more scanty in hepatocellular carcinomas. The number of both types showed a significant positive correlation with the degree of tumor fibrosis. The peritumoral ASMA-positive perisinusoidal cells were frequently in direct continuity with intratumoral ASMA-positive stromal cells in cholangiocarcinomas and metastatic liver carcinomas. CONCLUSIONS: These findings show that ASMA-positive stromal cells are related to tumor fibrosis in liver malignancies. Although direct evidence is lacking, the data suggest that, in cholangiocarcinomas and metastatic liver carcinomas, peritumoral ASMA-positive perisinusoidal cells transform into activated perisinusoidal cells (myofibroblasts), are incorporated into the tumor (intratumoral ASMA-positive stromal cells), and produce extracellular matrix proteins, that lead to tumor fibrosis. The scanty ASMA-positive cells in hepatocellular carcinomas may in part be responsible for the small amount of fibrosis in this tumor.

Actins↗
PubMed1996

Expression of blood group-related antigens in cholangiocarcinoma in relation to non-neoplastic bile ducts.

The abnormal expression of blood group related antigens has been reported in many malignant tumours; however, such expression in cholangiocarcinoma has not been examined systematically. The expression of blood group-related antigens (A, B, H, Lewis(a), Lewis(b), Lewis(x), Lewis(y), carbohydrate antigen 19-9 and carcinoembryonic antigen) was investigated immunohistochemically in 75 cases of cholangiocarcinoma (31 peripheral type and 44 hilar type). In non-neoplastic bile ducts, A, B, and H antigens were expressed in large bile ducts, while Lewis(a,b,y) and carbohydrate antigen 19-9 were variably expressed in both large and small bile ducts. Lewis(x) and carcinoembryonic antigen was not found in non-neoplastic bile ducts. In cholangiocarcinomas, A, B, and H, antigens were more frequent in the hilar type than in the peripheral type, although the difference was not significant. The expression of the blood-group related antigens, particularly A, Lewis(a,b,y), carcinoembryonic antigen, and carbohydrate antigen 19-9, was frequent in the tumour cells in well differentiated adenocarcinomas, while their immunoreactivity was less frequent in poorly differentiated adenocarcinomas. The superanuclear and luminal expression of these antigens in carcinoma cells was frequent in well differentiated adenocarcinomas, and the diffuse, cell membranous and stromal expression of these antigens was relatively frequent in poorly differentiated adenocarcinomas and adenosquamous carcinoma. The A, B, and H immunoreactivity of both non-neoplastic bile ducts and cholangiocarcinomas was consistent with the host blood group type. These findings suggest that both the expression and intracellular distribution of blood group-related antigens in cholangiocarcinoma are related to the differentiation of cholangiocarcinoma and, possibly, to the parent structure.

ABO Blood-Group System↗
PubMed1996

Histopathology of the liver in non-cirrhotic portal hypertension of unknown aetiology.

Non-cirrhotic, long-standing portal hypertension of unknown aetiology is being re-evaluated histopathologically and clinically. In this study, we examined 107 livers with this condition (92 wedge biopsy and 15 autopsy specimens) from five institutions in Japan. These cases were histologically categorized into four groups: idiopathic portal hypertension (66 cases), nodular regenerative hyperplasia (14 cases), partial nodular transformation (two cases), and incomplete septal cirrhosis (25 cases). These four groups shared several histological features: dense portal fibrosis with portal venous obliteration and intralobular slender fibrosis. In addition, the histopathological features characteristic of one group were also found to a mild degree in other groups. The histopathological lesions preceding portal venous obliteration remain speculative. However, the portal venous obliteration may be responsible for the occurrence of sustained portal hypertension and several of the pathological changes in these livers. It seems likely that idiopathic portal hypertension, nodular regenerative hyperplasia, partial nodular transformation and incomplete septal cirrhosis comprise a family of non-cirrhotic, long-standing portal hypertension in Japan, and the histological differences between them may reflect chronological progression of a single disease.

Adolescent↗
PubMed1996

An immunohistochemical study of tumour vessels in metastatic liver cancers and the surrounding liver tissue.

To elucidate the phenotype of the blood vessels and the expression of the growth factors involved in angiogenesis in metastatic liver cancers, we carried out an immunohistochemical study of 57 surgically resected livers with metastatic cancer. Blood vessels in the metastatic liver cancers frequently expressed von Willebrand factor (vWF), Ulex europaeus agglutinin I (UEA I)-binding sites, alpha-smooth muscle actin (alpha-SMA), type IV collagen and laminin. Sinusoidal endothelial cells around the metastatic liver cancers were positive for vWF in 33.3% of the specimens examined and for UEA I in 28.1%. alpha-SMA-positive perisinusoidal cells accumulated in the vicinity of the metastatic liver cancers in 68.4% of the specimens. Type IV collagen was detected in the perisinusoidal space close to the metastatic cancers as well as distant from them (91.2%). Laminin was detected in the perisinusoidal space in only one specimen (1.8%). Tumour cells of the metastatic liver cancers were positive for vascular endothelial growth factor, basic fibroblast growth factor (bFGF), and acidic fibroblast growth factor (aFGF) in 78.9%, 38.4% and 7.0% of the specimens, respectively. Hepatocytes close to the metastatic liver cancers expressed bFGF more strongly than those distant from the metastatic liver cancers, and their expression of bFGF was more intense than that in the tumour cells. These results suggest that: (1) tumour vessels in metastatic liver cancers consist of endothelium, basement membrane and pericytes, (2) the sinusoids adjacent to tumours undergo capillarization, and (3) vascular endothelial growth factor may contribute to angiogenesis in metastatic liver cancer. Basic fibroblast growth factor may be responsible for the sinusoidal capillarization and the peritumoral fibrosis.

Fibroblast Growth Factors↗
PubMed1996

Expression of immunoreactive matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases in human normal livers and primary liver tumors.

Matrix metalloproteinases (MMPs) play an important role in cancer cell invasion by degrading extracellular matrix proteins. However, little is known about the in situ expression of MMP in human normal livers and primary liver tumors. In this study, we therefore examined the in situ expression of immunoreactive MMP and tissue inhibitors of MMP (TIMP) in 10 normal livers, 11 surgically resected intrahepatic cholangiocarcinomas (CCs), and 6 surgically resected hepatocellular carcinomas (HCCs). In normal livers, MMP and TIMP were infrequently and faintly expressed in bile ducts, but were not expressed in hepatocytes. In the 11 CCs, MMP-1, MMP-2, MMP3, MMP-9, TIMP-1, and TIMP-2 were expressed in tumor cells and/or tumor stroma in 11 (100%), 5 (45%), 8 (73%), 3 (27%), 9 (82%), and 9 (82%), respectively. The expression of MMP and TIMP in tumor cells was located in the cytoplasm with a diffuse or granular pattern; that in the tumor stroma was situated in fibroblasts, leukocytes, and extracellular matrix. Their expression was stronger in CC cases with severe invasion than in CC cases with mild invasion. In contrast, MMP and TIMP were not expressed in any cases of HCC. These results show that intrahepatic bile duct cells may neoexpress or overexpress MMP and TIMP after malignant transformation but that hepatocytes do not, and suggest that MMP and TIMP play an important role in CC cell invasion by degrading extracellular matrix proteins.

Adult↗
PubMed1996

A morphometric and immunohistochemical study on angiogenesis of human metastatic carcinomas of the liver.

BACKGROUND/AIMS: To clarify the angiogenetic process and the origin of tumor vessels in human metastatic liver carcinomas. METHODS: One hundred autopsy livers with metastatic carcinomas were studied by immunohistochemistry for von Willebrand factor, by lectin histochemistry for Ulex europaeus agglutinin I (UEA-I), and by morphometry of the density of tumor vessels in the liver metastases. In addition, tumor vessels were observed three-dimensionally in silicone rubber-injected livers with metastases. RESULTS: Tumor vessels in metastatic liver carcinomas were positive for von Willebrand factor and UAE-I agglutinin I receptor. Tumor vessels first appeared in liver metastases of 200 micron in diameter. The density of the tumor vessels in the metastases increased up to 3mm in diameter, and it remained stable over 3mm. Sinusoidal endothelial cells around the liver metastases were positive for these endothelial markers. Sinusoidal endothelial cells were frequently in continuity with vessels in the metastases. Silicone rubber-injected specimens showed that blood vessels arising from surrounding sinusoids entered into the metastases. CONCLUSIONS: The angiogenesis of liver metastases may progress stepwise as the metastases enlarge, and capillarization of sinusoidal endothelium around the liver metastases may occur. Tumor vessels of liver metastases may in part originate from sinusoidal endothelial cells neighboring the tumors.

Humans↗
PubMed1996

Expression of mucin carbohydrate antigens (T, Tn and sialyl Tn) and MUC-1 gene product in intraductal papillary-mucinous neoplasm of the pancreas.

Aberrant or incomplete glycosylation of mucins results in expression of T, Tn, and sialyl-Tn (STn) antigens in various malignant neoplasms. MUC-1 gene product (a mucin core protein of mammary type) is known to alter or overexpress in several malignant tumors. However, expression of these mucin-related antigens has rarely been examined in intraductal papillary-mucinous neoplasm (IPN) of the pancreas. The authors examined immunohistochemically the expression of these antigens and MUC-1 gene product in nine IPN. In normal pancreas (n = 5), pancreatic ducts did not express T, Tn, or STn antigens, but expressed MUC-1 gene product. Among the nine IPNs, two (22%) expressed T antigen, nine (100%) expressed Tn antigen, and seven (78%) expressed STn antigen. MUC-1 gene product was expressed in nine (100%) IPNs. In invasive ductal adenocarcinoma of the pancreas (n = 6), all cases showed strong expression of Tn and STn antigens and the MUC-1 gene product, but expressed no T antigen. The expression of these antigens and MUC-1 gene product was focal in IPN, whereas it was diffuse in invasive ductal adenocarcinoma of the pancreas. These data suggest that aberrant or incomplete glycosylation occurs in epithelial mucins of IPN, that IPN is a borderline or low grade malignant neoplasm in terms of mucin-related antigen expression, and that mucin core protein (MUC-1 gene product) does not alter during pancreatic ductal carcinogenesis.

Adenocarcinoma, Papillary↗
PubMed1996

Histologic growth patterns of metastatic carcinomas of the liver.

One hundred autopsied livers containing metastatic cancers were studied pathologically. Macroscopically, the cancers were of the multinodular type in 65.0% of cases, massive type in 17.0% and portal tract type in 8.0%. Among liver metastases from colon and lung cancers, most cases showed predominantly intraparenchymal growth (92.3% and 87.5%, respectively). In contrast, among liver metastases from gallbladder/bile duct cancer, intraparenchymal growth was less frequent (35.7%). With regard to the histologic growth pattern at the boundary of the liver metastases, in micrometastases less than 1 mm in diameter a replacement growth pattern was predominant among metastases from lung, colon and pancreas cancers (69.7%, 79.3% and 66.7%, respectively), whereas a sinusoidal growth pattern was predominant in those from gastric and gallbladder/bile duct cancers (48.5% and 66.7%). Among macrometastases of the liver over 20 mm in diameter, an expansive growth pattern was predominant, irrespective of the cancer primary site. Thus metastatic liver cancers showed changes in growth patterns according to the size of the metastatic tumors.

Aged↗
PubMed1996

Expression of oncogene products, anti-oncogene products and oncofetal antigens in intraductal papillary-mucinous neoplasm of the pancreas.

A few previous studies have demonstrated the expression or mutations of oncogenes and anti-oncogenes as well as that of oncofetal antigens in intraductal papillary-mucinous neoplasm of the pancreas. In this study, we have investigated the immunohistochemical expression of oncogene (ras and c-erbB-2) and anti-oncogene (p53 and retinoblastoma [Rb]) products and oncofetal antigens (CEA, CA19-9 and DUPAN-2) in nine such tumours of the pancreas. In normal pancreas (5 cases), the Rb gene product and CA19-9 were expressed in all cases, while ras and c-erbB-2 gene products, p53 protein, CEA and DUPAN-2 were not expressed. In intraductal papillary-mucinous tumours (n = 9), ras, c-erbB-2, p53 and Rb gene products were present in 4/9 (44%), 7/9 (78%), 0.9 (0%) and 6/9 (67%) cases, respectively. CEA, CA19-9 and DUPAN-2 were expressed in 8/9 (89%), 9/9 (100%) and 2/9 (22%) cases respectively. In invasive ductal adenocarcinoma of the pancrease (7 cases), ras, c-erbB-2, p53 and Rb gene products were expressed in 3/7 (43%), 6/7 (86%), 2/7 (29%) and 3/& (43%) cases respectively. CEA, CA19-9 and DUPAN-2 were expressed in 7/7 (100%), 7/7 (100%) and 6/7 (86%) cases, respectively. The extent and intensity of the expression of these antigens was greater in invasive ductal adenocarcinomas. These data suggest that activation of ras and c-erbB-2 oncogenes and inactivation of Rb anti-oncogene may contribute to the development and progression of intraductal papillary-mucinous tumours of the pancreas and that there is neo-expression of CEA and DUPAN-2 during the development and progression of these tumours.

Adenocarcinoma, Mucinous↗
PubMed1996

Expression of apoptosis, proliferating cell nuclear antigen, and apoptosis-related antigens (bcl-2, c-myc, Fas, Lewis(y) and p53) in human cholangiocarcinomas and hepatocellular carcinomas.

In situ expression of apoptosis and its related antigens has rarely been evaluated in human liver tumors. Therefore, investigation using in situ nick end-labeling and immunohistochemical methods of the in situ expression of apoptosis, proliferating cells, and apoptosis-related antigens in 7 normal livers, 20 cholangiocarcinomas (CC) and 17 hepatocellular carcinomas (HCC) was done. Apoptotic cells as determined by the nick end-labeling method and proliferating cell nuclear antigen-positive cells were present in all specimens, and the percentage of them was significantly higher in CC than in HCC. Bcl-2 protein was present only in one CC and one HCC, but was occasionally noted in bile ducts in non-cancerous livers. C-myc and Fas antigens were not found in any of the cases. Lewisy antigen was expressed in 8 CC, but was absent in the other cases although bile ducts in non-cancerous livers frequently expressed Lewisy. p53 protein was present in 8 CC, but was absent in the other cases. Serial section observations showed that apoptotic cancer cells were consistently negative for proliferating cell nuclear antigen; bcl-2-positive cells did not show apoptosis; p53-positive cancer cells showed apoptosis. Some Lewisy-positive cancer cells showed apoptosis, while others did not. These data suggest that apoptosis and cell proliferation are involved in CC and HCC, and their degree is more severe in CC than in HCC. p53 protein (stimulative) may regulate apoptosis in some cases, whereas c-myc, Fas and Lewisy are not related to apoptosis in CC and HCC in vivo. Many other factors may regulate apoptosis in CC and HCC in vivo.

Apoptosis↗