Publications by authors named "Joh T"

Goals: To examine the safety and effectiveness of percutaneous radio-frequency ablation therapy (PRAT) for malignant liver tumors, using a needle with cluster radio-frequency (RF) electrodes.

Study: The subjects were 13 patients with solitary malignant liver tumors: 10 had hepatocellular carcinoma and 3 had metastatic liver tumors. One session of PRAT with cluster RF electrodes was performed until roll-off occurred two times.

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Alpha-fetoprotein (AFP) producing gastric cancer (AFP-GC) is very malignant and highly metastatic compared with common gastric cancer. However, the causal relationship between AFP production and the high malignancy of AFP-GC is unclear. We investigated AFP gene regulation in AFP-GC by an active transcription factor, HNF1 (hepatocyte nuclear factor 1) and a repressive transcription factor, ATBF1 (AT motif binding factor 1).

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Background/aims: The aim of the present study was to examine the safety and effectiveness of percutaneous radiofrequency ablation therapy using a needle with cluster radiofrequency electrodes in an animal model.

Methodology: A total of 10 radiofrequency applications were performed in the normal liver of 5 domestic pigs with real-time ultrasonography until roll-off occurred two times. Aspartate aminotransferase, alanine aminotransferase, lactic dehydrogenase, and total bilirubin were evaluated before the procedure and 1 h, 24 h, and 7 days following percutaneous radiofrequency ablation therapy.

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Background And Aims: E-cadherin, which is a [Ca2+]-dependent, homotypic cell-cell adhesion molecule, is expressed in gastrointestinal epithelial cells. Much has been learned about the down-regulation of E-cadherin expression in gastrointestinal tumours, Barrett's oesophageal dysplasia, and Crohn's disease, but the functions of this molecule in normal gastrointestinal mucosa are less known.

Methods: In this study, we investigated the relationship between E-cadherin expression and permeability using rat cultured gastric and intestinal epithelial cells following a 30-min exposure to various pH solutions.

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Excessive proinflammatory cytokine and NO production by activated microglia play a role in neurodegenerative disorders. To investigate whether the neuroprotectant N-acetyl-O-methyldopamine (NAMDA) downregulates genes associated with microglial activation, we measured gene expression of TNF-alpha, IL-1beta, inducible nitric oxide synthase (NOS2), and an associated cofactor synthesis gene, GTP cyclohydrolase I (GTPCH) in LPS-stimulated microglia cells in the presence or absence of NAMDA. The temporal pattern of cytokine gene expression showed that LPS (0.

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Inflammatory bowel disease (IBD) is associated with Th1/Th2 cytokine dysregulation, leukocyte extravasation, and tissue edema, but the mechanisms for cytokine-mediated vascular dysfunction are not understood. To investigate how cytokines might control edema in IBD, we determined vascular permeability and IFN-gamma expression in two models of murine colitis: SCID mice reconstituted with CD45RB(high T-lymphocytes (CD45RB(high)/SCID mice), and interleukin-10 gene deficient (IL-10(-/-)) mice. We also investigated the in vitro effects of IFN-gamma and IL-10 on human endothelial solute barrier and junction protein expression.

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Background/aims: To compare the effectiveness of different imaging modalities and the significance of tumor biopsy for diagnosing small hepatocellular carcinoma.

Methodology: Nodules (n = 352) with diameters of 30 mm or less newly detected by periodic ultrasonography and computed tomography in 234 patients with chronic liver disease were investigated with magnetic resonance imaging and digital subtraction angiography. These findings were compared with histologic findings.

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IL-18 is a pleiotropic cytokine also proposed to have a role in modulating immune function during stress. Initially found in immune cells, IL-18 mRNA is detectable in several tissues including the cells of the zona reticularis and the zona fasciculata of the adrenal cortex, where its levels are elevated by acute stress or adrenocorticotropic hormone treatment. In the present study, we compared the expression of IL-18 in the adrenal cortex with that of spleen and duodenum, two other IL-18-positive tissues.

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Background And Study Aims: Although endoscopic mucosal resection (EMR) for early gastric cancer (EGC) without ulceration or scarring has been very popular in Japan and thought to be beneficial, curability by EMR is still lower than that for surgical resection. We investigated patients whose EGCs were resected endoscopically in order to identify the factors affecting curability by EMR.

Patients And Methods: We investigated retrospectively 256 EGC lesions (251 patients) which were subjected to EMR between 1989 and 1998 with respect to patient profile, macroscopic type, location, maximum diameter of tumors, resection method and histological typing.

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The involvement of pancreatic acinar cell apoptosis and its relation to glucocorticoid exposure were investigated in spontaneously occurring chronic pancreatitis in male Wistar Bonn/Kobori (WBN/Kob) rats. Although most lobules were not inflamed in 10-week-old WBN/Kob, increased apoptosis of pancreatic acinar cells, confirmed by TUNEL staining was focally observed (0.10 +/- 0.

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We investigated the effect of DNA vaccines encoding H. pylori-heat shock protein A and B (pcDNA3.1-hspA and -hspB) on inducing immune responses against H.

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The nucleotide sequence of hiC12, isolated as a cDNA clone of hardening-induced Chlorella (hiC) genes, was identified. The clone encodes a late embryogenesis abundant (LEA) protein having six repeats of a 11-mer amino acid motif, although in a slightly imperfect form. To overexpress the hiC61) and hiC12 genes, their coding regions were PCR amplified and subcloned into a pGEX-1lambdaT vector.

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Evidence is accumulating that gap junctional intercellular communication (GJIC) plays an important role in the gastric mucosal defense system. This study was conducted to determine whether GJIC mediates a restitution process in gastric mucosa. Male Sprague-Dawley rats were fasted and anesthetized.

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Phytases are the primary enzymes responsible for the hydrolysis of phytic acid, myo-inositol-1, 2, 3, 4, 5, 6-hexakisphosphate (InsP6). The pathway of hydrolysis of InsP6 by phytase from wheat bran of Triticum aestivum L. cv.

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Lactacystin (LC) is a specific inhibitor of the proteasome, and has recently been shown to induce apoptosis in certain cell lines. In the present study, we established Fas-resistant adult T-cell leukemia (ATL) cell subclones RSO4 and RST1 from their parental Fas-sensitive cell lines SO4 and ST1, and examined whether LC can overcome Fas resistance. LC completely inhibited proteasome function as determined by a peptidyl-MCA substrate (LLVY-MCA and LLE-MCA), and induced apoptosis in these cell lines irrespective of Fas sensitivity at low concentrations (approximately 10 microM).

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Interleukin (IL)-18 is a proinflammatory cytokine and a stimulator of cell-mediated immune responses. We have previously reported that acute stress stimulates the production of IL-18 mRNA in the glucocorticoid (GC)-producing cells of the adrenal cortex. In order to investigate the mechanisms governing the expression of IL-18 in the adrenal cortex, the effects of acute ACTH or chronic corticosterone treatment on the levels of IL-18 mRNA and protein were examined by in situ hybridization and Northern and Western blot assays.

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Objective: HIV-1 infection is associated with alterations of several vascular endothelial functions including adhesion molecule expression, growth, and vascular permeability. The bases of these errors are not known, but might involve secretion of the HIV-1 derived transcription factor 'Tat-1'. This study investigated Tat-1 mediated endothelial barrier changes and second message regulation of this phenomenon.

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SATB1 is expressed primarily in thymocytes and can act as a transcriptional repressor. SATB1 binds in vivo to the matrix attachment regions (MARs) of DNA, which are implicated in the loop domain organization of chromatin. The role of MAR-binding proteins in specific cell lineages is unknown.

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We present a case that suggests a relationship between primary biliary cirrhosis and myasthenia gravis. A 43-year-old Japanese woman was admitted to the Nagoya City University Medical School, First Department of Internal Medicine with abnormal liver function in August 1991. She had had ptosis of the right eye since 1990.

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A preventive role for human T-cell leukemia virus type-I (HTLV-I) and Fas-associated phosphatase-1 (FAP-1) in Fas-mediated apoptosis has been reported in HTLV-I-infected cells. In the present study, we examined whether these molecules increased during the acquisition of Fas-resistance in adult T-cell leukemia (ATL) cell lines. SO4, ST1 and KK1 are Fas-sensitive ATL cell lines, and produce small amounts of HTLV-I in vitro.

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Background/aims: To determine the safety and effectiveness of endoscopic injection sclerotherapy (EIS) for children with biliary atresia.

Methodology: Subjects were 7 patients with biliary atresia with esophagogastric varices and variceal bleeding. Intravariceal injection using 5% ethanolamine oleate was performed under fluoroscopy until varices were eradicated.

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A complement regulatory protein, decay-accelerating factor (DAF, CD55), is known to protect host tissues from autologous complement activation. DAF is present on the apical side of human gastric epithelial cells, and its expression increases during gastritis. To develop an animal model for analysis of DAF expression on gastric cells, a mAb to guinea pig DAF was successfully used.

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This is the first study to demonstrate that the AT motif binding factor 1-A (ATBF1-A) is expressed in the crypts and the bases of villi of the small intestine and negatively regulates transcription of brush-border enzyme gene, aminopeptidase-N (APN). In situ hybridization visualized a limited ATBF1-A mRNA expression in the crypts and the bases of villi. Transient transfection and dual luciferase-reporter assay demonstrated that ATBF1-A suppressed the activity of APN promoter, but did not that of AT motif deleted promoter.

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