A Terano

The University of Tokyo, Tokyo, Tokyo-to, Japan

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Publications (182)809.99 Total impact

  • A Terano, S Ota, H Hiraishi, H Mutoh
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    ABSTRACT: In 1979, a new mechanism of gastric defense named cytoprotection was followed by numerous reports elucidating this interesting and important phenomenon. During this decade, however, the concept and definition of gastric cytoprotection have been modified from the morphological and ultrastructural viewpoints. This review attempts to describe the concept and mechanisms of cytoprotection as well as its pathophysiological features. Specifically, in vitro studies using isolated cells or monolayer cultured cells as well as molecular investigations of signal transduction system have been documented.
    Acta pathologica japonica 01/2008; 43(1-2):2-10.
  • Endoscopy 03/2007; 39 Suppl 1:E243-4. · 5.74 Impact Factor
  • Journal of Gastroenterology and Hepatology 01/2007; 22(9):1551-1551. · 3.33 Impact Factor
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    ABSTRACT: Trefoil factor family (TFF) is a group of small peptides secreted by gastrointestinal epithelial cells.Among three known TFF peptides, TFF1 (formerly pS2) is expressed at a high level in gastric epithelial cells and plays an essential and critical role in maintaining the integrity of the gastric mucosa. Recent evidence also suggests that TFF1 acts as a tumour suppressor gene in the stomach.TFF1 was originally discovered as an oestrogen-inducible gene in MCF-7 breast cancer cells, and its expression is dependent on oestrogen in MCF-7 and other hormone-dependent breast cancer cells. Although gastric epithelial cells express oestrogen receptors (ERs), gastric TFF1 expression appears to be independent of oestrogen signalling. Instead, several cis-regulatory elements are involved in the regulation of gastric TFF1 expression and balanced signalling from gp130, a common IL-6 family coreceptor, has been shown to be necessary for the proper expression of TFF1 in the stomach.Epigenetic regulation, such as DNA methylation in the promoter region of the TFF1 gene, may be also important for tissue-specific expression of TFF1 in the stomach. However, further studies are still needed to fully understand the detailed regulatory mechanisms of TFF1 expression in gastric epithelial cells.
    Alimentary Pharmacology & Therapeutics Symposium Series 06/2006; 2(1):285 - 291.
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    ABSTRACT: The majority of gastro-oesophageal reflux disease (GERD) seems to be non-erosive reflux disease. Nonerosive reflux disease includes minimal change oesophagitis (whitish or reddish, oedematous change and erosion that is not regarded as mucosal break) and no endoscopic abnormalities. To investigate the accurate proportion of those with minimal change oesophagitis and to clarify its characteristics. In addition, we evaluated the effect of famotidine (40 mg/day) in those with minimal change. Prospective endoscopic assessment was performed for consecutive 606 out-patients. Of the 582 patients suitable for analysis, 347 were non-treated. The latter were divided into those with erosive GERD or minimal change, and their endoscopic findings and characteristics were compared. Among 347 non-treated patients, 88 (25%) had erosive GERD and 249 (72%) had minimal change. Compared with patients who have erosive GERD and those with minimal change, the latter were less likely to have hiatal hernia or bile reflux, but more likely to have gastric atrophy. Symptomatic patients (n = 55) with minimal change oesophagitis were more likely to have hiatal hernia than those who were asymptomatic (n= 194). Most patients preferred taking famotidine on-demand, during a 4-week follow-up period. Most non-erosive reflux disease can be classified as minimal change oesophagitis, and that have different characteristics from erosive GERD. On-demand famotidine may be a suitable alternative treatment for patients with minimal change disease.
    Alimentary Pharmacology & Therapeutics 07/2005; 21 Suppl 2:19-26. · 4.55 Impact Factor
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    ABSTRACT: Corticotropin releasing factor (CRF) is distributed in the central nervous system and acts as a neurotransmitter to regulate gastric functions through vagal-muscarinic pathways. We have recently demonstrated that central CRF aggravates experimental acute liver injury in rats. In the present study, the central effect of CRF on hepatic circulation was investigated. Hepatic surface perfusion was determined by laser Doppler flowmetry in urethane anaesthetised rats. Portal pressure and portal blood flow was simultaneously monitored. CRF (0.1-4 nmol), urocortin II (a selective CRF2 receptor agonist 2.5-100 pmol), or saline vehicle was injected intracisternally, and changes in hepatic circulation were observed for 120 minutes. We examined the effects of various pretreatments with K41498, a selective CRF2 receptor antagonist, atropine, 6-hydroxydopamine, hepatic plexus denervation, or hepatic branch vagotomy, respectively. Intracisternal injection of CRF (0.2-4 nmol) caused a dose dependent decrease in hepatic surface perfusion with a maximum response occurring 60 minutes post injection. Portal pressure was dose dependently elevated and portal blood flow was decreased by intracisternal CRF concurrently with the decrease in hepatic surface perfusion. These changes in hepatic circulation by intracisternal CRF were abolished by 6-hydroxydopamine and hepatic plexus denervation, but not by atropine or hepatic vagotomy. Urocortin II injected intracisternally decreased hepatic surface perfusion and elevated portal pressure at doses within the picomolar range. Intracisternal preadministration of K41498 inhibited the effect of central CRF on the hepatic circulation. These data suggest that CRF acts in the brain to decrease hepatic surface perfusion and elevate portal pressure through central CRF(2) receptor and sympathetic-noradrenergic pathways.
    Gut 03/2005; 54(2):282-8. · 10.73 Impact Factor
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    ABSTRACT: Aim:  Trefoil factor family (TFF) peptides are known to facilitate wound healing in gastric mucosa. However, the regulatory mechanisms of gastric TFF expression are not fully understood yet. In this study, we examined the effect of TNF-α on TFF1 and TFF2 expression in gastric epithelial cells.Methods:  MKN45 cells were used. TFF mRNA expression was analyzed by real-time quantitative RT-PCR. Promoter sequences of TFF1 gene (−956 to +36) and TFF2 gene (−912 to +24) were inserted into pGL3 vector and reporter gene assays were performed. NF-κB activity was monitored by using a NF-κB responsive element-driven reporter vector.Results:  (1) TNF-α(0.1–30 ng/ml) down-regulated TFF1 and TFF2 mRNA expression in a dose-dependent manner. (2) Reporter gene assays also confirmed the down-regulation of TFF1 and TFF2 gene transcription by TNF-α. (3) TNF-α activated NF-κB. (4) Overexpression of dominant negative IκBα prevented both TNF-α-induced NF-κB activation and TNF-α-induced down-regulation of TFF expression.Conclusions:  TNF-α down-regulates gastric TFF expression through NF-κB pathway, suggesting that TFF expression is sensitive to inflammatory stimuli.
    Wound Repair and Regeneration 01/2005; 13(1):A5 - A5. · 2.76 Impact Factor
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    ABSTRACT: Recent evidence suggests that peripheral blood granulocytes and monocytes/macrophages have a major role in the exacerbation of ulcerative colitis. Our objective was to investigate if selective granulocyte and monocyte adsorptive apheresis with Adacolumn promotes remission of active ulcerative colitis and spares corticosteroid. Sixty patients with active ulcerative colitis were studied, of whom 39 had relapsing-remitting ulcerative colitis, 15 had chronic continuous and 6 had their first episode of ulcerative colitis. Granulocytapheresis was done with an Adacolumn filled with cellulose acetate beads as apheresis carriers that adsorb FcgammaR and complement receptors bearing leucocytes (granulocytes, monocytes and a small fraction of lymphocytes). Patients received up to 10 Adacolumn sessions over 12 weeks, one session was 60-90 min at 30 mL/min. No additional medication was given. Efficacy was assessed with Seo's activity index (AI) [Seo M, Okada M, Yao T. An index of disease activity in patients with ulcerative colitis. Am J Gastroenterol 1992;87:971-6]. The mean AL was 197.5 and range 154.4-277.7. AI < 150 was considered significant improvement and AI < 100 was considered clinical remission. Of 60 patients, 50 (83.3 %) improved, 14 achieved remission, granulocytapheresis was most effective in steroid-dependent patients. At entry, the mean dose of prednisolone was 15.3 mg/day per patient and was reduced to 3.6 mg/day after 10 sessions. Granulocytapheresis was well tolerated and no serious side-effects were observed. Based on our experience in patients with diverse ulcerative colitis disease expression and long-term exposure to conventional drug therapy, we believe that granulocytapheresis is an effective adjunct to conventional medication for promoting remission and sparing steroids in patients with active ulcerative colitis.
    Digestive and Liver Disease 12/2004; 36(12):811-7. · 3.16 Impact Factor
  • Journal of Gastroenterology and Hepatology 10/2004; 19(9):1081. · 3.33 Impact Factor
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    ABSTRACT: Trefoil factor family peptides are expressed in gastrointestinal epithelial cells and play a critical role in maintaining mucosal integrity. Although non-steroidal anti-inflammatory drugs (NSAIDs) are important causative agents of gastric mucosal lesions, few data are available about the effect of NSAIDs on trefoil family peptides in gastric mucosa. To examine whether indometacin, a widely used NSAID, affects trefoil factor family expression in gastric epithelial cells. MKN45, a cell line derived from human gastric cancer, was used. TFF1, TFF2, and TFF3 mRNA expression was assessed by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). TFF2 gene transcription was also examined by luciferase reporter gene assay. Relative expression level of TFF1, TFF2, TFF3 mRNA was 616: 12: 1 in unstimulated MKN45 cells. Although indometacin (1-250 micro mol/L) had no significant effect on the expression of TFF1 and TFF3 mRNA, it up-regulated TFF2 mRNA expression in a dose- and time-dependent manner. Luciferase reporter gene assay confirmed the up-regulation of TFF2 gene transcription by indometacin. Indometacin-induced up-regulation of TFF2 expression was not antagonized by externally applied prostaglandin E2. These results suggest that indometacin up-regulates gastric epithelial cell TFF2 expression through a COX-independent mechanism. Since TFF peptides play an important role in gastric mucosal protection, indometacin-induced TFF2 may reduce the degree of gastric mucosal damage induced by indometacin.
    Alimentary Pharmacology & Therapeutics 08/2004; 20 Suppl 1:171-6. · 4.55 Impact Factor
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    ABSTRACT: The incidence of gastroduodenal diseases is high in patients with chronic renal failure (CRF). However, gastric acidity in CRF has been reported to range in level from low to high. Moreover, it remains unknown whether Helicobacter pylori infection influences gastric acidity in such patients. Thus, we aimed to clarify the pathophysiological perturbation in gastric acidity and to determine the influence of H. pylori infection in CRF. Case-control study. A university hospital. Twenty-seven patients with CRF and 24 control patients, presenting with either gastrointestinal symptoms, positive faecal occult blood, or anaemia (haemoglobin <10 g dL(-1)). The patients underwent gastroduodenal endoscopy with simultaneous determination of H. pylori infection. Gastric ammonium concentration, serum pepsinogen I and II, and basal gastrin level were measured. Thereafter, gastric acid secretion was monitored by 24-h intragastric acidity measurement with calculation of pH-3 holding time (%) (hours showing pH>3/24 h). In the CRF group, pH-3 holding time of H. pylori (+) subgroup was significantly greater than that of H. pylori (-) subgroup (71.2 +/- 32.4% vs. 32.8 +/- 30.0%, mean +/- SD; P=0.03). Pepsinogen I/II ratio was inversely correlated with pH-3 holding time in the control and CRF groups. Gastric ammonium concentration in CRF/H. pylori (+) subgroup (14.1 +/- 9.2 mmol L(-1)) was significantly higher than in CRF/H. pylori (-) (2.5 +/- 2.7 mmol L(-1); P=0.002) and control/H. pylori (+) subgroups (6.1 +/- 4.2 mmol L(-1); P=0.01). Serum gastrin level was significantly higher in the CRF group than in the control group (297 +/-343 pg mL(-1) vs. 116 +/- 69 pg mL(-1); P=0.02) as a whole. However, there was no significant correlation between serum creatinine and gastrin levels in the CRF group. Gastrin level in CRF/H. pylori (+) subgroup was significantly higher than in CRF/H. pylori (-), control/H. pylori (+), and control/H. pylori (-) subgroups (423 +/-398 pg mL(-1) vs. 113 +/- 79, 124 +/- 78, and 96 +/-43 pg mL(-1), respectively; P=0.01-0.03). Significant positive correlations amongst pH-3 holding time, ammonium and gastrin concentrations were found in the CRF group, but not in the control group. CRF without H. pylori infection primarily shows a tendency for high gastric acidity, but without hypergastrinaemia. Persistent H. pylori infection in CRF leads to decreased acidity and, consequently, to fasting hypergastrinaemia via a feedback mechanism. The hypoacidity in CRF with H. pylori infection appears to result from neutralization of acid by ammonia as well as from gastric atrophy. Thus, H. pylori infection status critically determines perturbation in gastric acidity and fasting gastrin level in CRF.
    Journal of Internal Medicine 11/2003; 254(5):439-46. · 6.46 Impact Factor
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    ABSTRACT: Although trefoil factor family peptides (TFF peptides) are assumed to play important roles in gastric mucosal protection, the regulatory mechanism of gastric TFF expression has not been fully understood yet. Recent reports showed gastric expression of peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor known to be involved in the regulation of cell growth and differentiation in other cell types, such as adipocytes. To determine whether PPARgamma affects the expression of TFF in gastric epithelial cells. MKN45 gastric cells were used as a model of gastric epithelial cells. DNA synthesis of the cells was determined by the measurement of BrdU incorporation. The effects of PPARgamma ligands, 15-deoxy-Delta12,14-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ) on TFF expression were assessed by real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR). MKN45 cells expressed a significant amount of PPARgamma. Both 15d-PGJ2 and TGZ suppressed DNA synthesis of the cells in a dose-dependent manner. In the control condition, MKN45 cells most abundantly expressed TFF1 and the relative expression level of TFF1, TFF2, and TFF3 mRNA was 1700:32:1. TFF1 and TFF2 mRNA levels were significantly up-regulated by the incubation of the cells with 15d-PGJ2 (10 micro m) or TGZ (30 micro m), whereas TFF3 mRNA level was not affected. The results of the present study suggest a possible role of PPARgamma in the regulation of TFF expression in gastric epithelial cells.
    Alimentary Pharmacology & Therapeutics 08/2003; 18 Suppl 1:119-25. · 4.55 Impact Factor
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    ABSTRACT: Résumé La photothérapie dynamique (PTD) est un traitement prometteur de traitement du néoplasme du tractus gastro-intestinal y compris du cancer gastrique. Un essai clinique de PTD (associé aux dérivés de l’hématoporphyrine et au laser argon) a été entrepris en 1979 sur le cancer gastrique au début. La PTD utilisant le porfimère sodé (PHE, Photofrin II lyophilisé), et un laser pulsé excimer (EDL) a été approuvée par le gouvernement japonais en 1996. L’indication de PTD dans les cancer gastriques au début est unique au Japon. La muco-résection endoscopique (ME) est considérée comme le traitement de première intention pour le cancer gastrique au début mais ses indications sont limitées au carcinome intramuqueux. En outre, des complications sévères telles la perforation peuvent survenir. D’autre part, la PTD est une technique sûre, qui améliore la qualité de vie du patient. Le développement de nouveaux photosensibilisateurs et de lasers plus appropriés ainsi que l’amélioration de la technique de PTD rendent les traitements plus efficaces non seulement pour les cancers gastriques au début mais aussi à des stades avancés. Summary PDT (photodynamic therapy) is a promising treatment for neoplasm in the gastrointestinal tract including gastric cancer. Clinical trial of PDT (combination of hematoporphyrin derivative and an argon dye laser) for early gastric cancer started in 1979. PDT using porfimer sodium (PHE, freeze-dried Photofrin II) and a pulsed excimer dye laser (EDL) was approved by government of Japan in 1996. Early gastric cancer is indicated for PDT only in Japan. Endoscopic mucosal resection (EMR) is considered the first choice treatment in early gastric cancer but its indication is limited to intramucosal carcinoma. Moreover, sometimes serious complications such as perforation occur. On the other hand, PDT has no serious complications and contributes to patient’s quality of life. Development of new photosensitizers and more effective lasers, and improvement of technique in PDT will enable more effective treatment for not only early stage but also advanced gastric cancers.
    Acta Endoscopica 01/2003; 33(4):521-529. · 0.16 Impact Factor
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    ABSTRACT: Involvement of peroxisome proliferator activated receptor gamma (PPARgamma) in the growth response of colon cancer cells has been suggested. To investigate the characteristics of PPARgamma induced apoptosis in colon cancer cells. The effects of ligands for each of the PPAR subtypes (alpha, delta, and gamma) on DNA synthesis and cell viability were examined in HT-29 colon cancer cells. Modulation of apoptosis related gene expression by PPARgamma ligands was screened with cDNA arrays, and the results were confirmed by quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis. PPARalpha, PPARdelta, and PPARgamma were all expressed in HT-29 cells. PPARgamma ligands, 15-deoxy-delta(12,)(14)-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ), suppressed DNA synthesis of HT-29 cells whereas ligands for PPARalpha and PPARdelta had no significant effects. Both 15d-PGJ2 and TGZ induced HT-29 cell death in a dose dependent manner which was associated with an increase in fragmented DNA and was sensitive to a caspase inhibitor. Among several genes selected by cDNA array screening, quantitative RT-PCR analysis confirmed downregulation of c-myc expression and upregulation of c-jun and gadd153 expression by 15d-PGJ2 and TGZ. PPARgamma induced apoptosis was antagonised by the presence of serum in the culture medium, and interaction between PPARgamma signalling and cell survival signalling through the phosphatidylinositol 3-kinase pathway was suggested. As c-myc is an important target gene of the adenomatous polyposis coli (APC)/beta-catenin and/or APC/gamma-catenin pathway, activation of PPARgamma signalling appears to compensate for deregulated c-myc expression caused by mutated APC. The present results suggest the potential usefulness of PPARgamma ligands for chemoprevention and treatment of colon cancers.
    Gut 06/2002; 50(5):658-64. · 10.73 Impact Factor
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    ABSTRACT: [corrected] Peroxisome proliferator-activated receptors (PPAR) are a family of three nuclear receptors (PPARalpha, PPARdelta, and PPARgamma). Although recent evidence suggests a role for PPARgamma in the regulation of colonic epithelial cell growth, the role for PPARgamma in the stomach has not been established. To examine the expression of PPARgamma and the effects of PPARgamma ligands on the viability of gastric epithelial cells. MKN45 cells and primary cultured rat gastric epithelial cells were used. Troglitazone (TGZ) and 15-deoxy-Delta12, 14-prostaglandin J2 (15d-PGJ2) were used as PPARgamma ligands. Expression of PPARgamma was examined by RT-PCR and Western blot analysis. Cell viability was measured by WST-1 assay and TUNEL assay was performed to detect apoptosis. MKN45 cells expressed all subtypes of PPAR. PPARgamma ligands decreased cell viability and induced cell death in a dose-dependent manner, whereas ligands for PPARalpha and PPARdelta had no significant effect. TUNEL assay showed that this cell death is apoptosis. Primary cultured rat gastric epithelial cells also expressed PPARgamma and activation of PPARgamma decreased cell viability. These results suggest that PPARgamma plays an important role in the regulation of cell growth and cell death in gastric epithelial cells.
    Alimentary Pharmacology & Therapeutics 05/2002; 16 Suppl 2:67-73. · 4.55 Impact Factor
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    ABSTRACT: Background: Involvement of peroxisome proliferator activated receptor γ (PPARγ) in the growth response of colon cancer cells has been suggested.Aims: To investigate the characteristics of PPARγ induced apoptosis in colon cancer cells.Methods: The effects of ligands for each of the PPAR subtypes (α, δ, and γ) on DNA synthesis and cell viability were examined in HT-29 colon cancer cells. Modulation of apoptosis related gene expression by PPARγ ligands was screened with cDNA arrays, and the results were confirmed by quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis.Results: PPARα, PPARδ, and PPARγ were all expressed in HT-29 cells. PPARγ ligands, 15-deoxy-δ12,14-prostaglandin J2 (15d-PGJ2) and troglitazone (TGZ), suppressed DNA synthesis of HT-29 cells whereas ligands for PPARα and PPARδ had no significant effects. Both 15d-PGJ2 and TGZ induced HT-29 cell death in a dose dependent manner which was associated with an increase in fragmented DNA and was sensitive to a caspase inhibitor. Among several genes selected by cDNA array screening, quantitative RT-PCR analysis confirmed downregulation of c-myc expression and upregulation of c-jun and gadd153 expression by 15d-PGJ2 and TGZ. PPARγ induced apoptosis was antagonised by the presence of serum in the culture medium, and interaction between PPARγ signalling and cell survival signalling through the phosphatidylinositol 3-kinase pathway was suggested.Conclusions: As c-myc is an important target gene of the adenomatous polyposis coli (APC)/β-catenin and/or APC/γ-catenin pathway, activation of PPARγ signalling appears to compensate for deregulated c-myc expression caused by mutated APC. The present results suggest the potential usefulness of PPARγ ligands for chemoprevention and treatment of colon cancers.
    Gut 01/2002; 50(5):658-664. · 10.73 Impact Factor
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    ABSTRACT: The epithelial cells of stomach are continuously exposed to various toxic agents that may cause mucosal injury. The epithelial lining is rapidly replaced by cells that migrate from the proliferative zone of the gastric gland, to maintain the integrity of the gastric mucosa. Thus, cell migration is an essential part of the early process of gastric mucosal repair. After various forms of gastric injury, mucosal integrity is reestablished by the rapid migration of epithelial cells. However, the cellular mechanisms of the restitution remain unclear to date. In this report, we will review the role of cellular migration in the repair process of gastric epithelial cells in culture. It has been reported that hepatocyte growth factor (HGF) has the potency of acceleration of cellular repair process. In this review, we also report that HGF plays a leading role in the mucosal repair after damage by using a novel cell culture model.
    Life Sciences 12/2001; 69(25-26):3083-9. · 2.56 Impact Factor
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    ABSTRACT: Non-alcoholic steatohepatitis is a distinct entity, characterized by fatty change, lobular inflammation and fibrosis of the liver. Some cases of non-alcoholic steatohepatitis progress to cirrhosis, but it is not easy to distinguish this disease from non-alcoholic fatty liver by non-invasive examinations. No proven therapy for non-alcoholic steatohepatitis exists. Transforming growth factor-beta1 is implicated in the development of liver fibrosis, and is inhibited by alpha-tocopherol (vitamin E) in the liver. Therefore, in this study, the significance of the measurement of the level of plasma transforming growth factor-beta1 and the effect of alpha-tocopherol on the clinical course of non-alcoholic steatohepatitis were investigated. Twelve patients with non-alcoholic steatohepatitis and 10 patients with non-alcoholic fatty liver, with a diagnosis confirmed by liver biopsy, were studied. None of the patients had a history of alcohol abuse, habitual medicine or malignant or inflammatory diseases. All patients were negative for hepatitis B, C and G virus. Patients were given dietary instruction for 6 months, and then alpha-tocopherol (300 mg/day) was given for 1 year. Blood chemistries, measurement of plasma transforming growth factor-beta1 level and liver biopsies were undertaken before and after the 1-year alpha-tocopherol treatment. The serum alanine transaminase level decreased in non-alcoholic fatty liver patients, but not in non-alcoholic steatohepatitis patients, after 6 months of dietary therapy. Although the serum alanine transaminase level in non-alcoholic steatohepatitis patients was reduced during the 1-year alpha-tocopherol treatment, alpha-tocopherol had no effect on the serum alanine transaminase level in non-alcoholic fatty liver patients. The histological findings, such as steatosis, inflammation and fibrosis, of the non-alcoholic steatohepatitis patients were improved after alpha-tocopherol treatment. The plasma transforming growth factor-beta1 level in non-alcoholic steatohepatitis patients was significantly elevated compared with that in non-alcoholic fatty liver patients and healthy controls, and decreased, accompanied by an improvement in serum alanine transaminase level, with alpha-tocopherol treatment. Our data suggest that the measurement of the level of plasma transforming growth factor-beta1 represents a possible method of distinguishing between non-alcoholic steatohepatitis and non-alcoholic fatty liver. Long-term alpha-tocopherol treatment may be safe and effective for non-alcoholic steatohepatitis. A randomized, controlled, double-blind trial is needed to confirm the full potential of alpha-tocopherol in the management of non-alcoholic steatohepatitis.
    Alimentary Pharmacology & Therapeutics 11/2001; 15(10):1667-72. · 4.55 Impact Factor
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    ABSTRACT: To elucidate the mechanisms of antiulcerogenic agents, we established the cell culture model derived from rat gastric epithelium. The cultured cells were identified as mucus-producing cells by using histological analysis. This culture model is useful for investigating the untiulcer effect of various agents and to reveal the mechanisms of the drug action. In particular, the ulcer-healing model using the cultured monolayer is promising and convenient for the study of several growth factors such as HGF as well as antiulcerogenic agents. The effect of polaporezinc in the cultured model is introduced.
    Microscopy Research and Technique 07/2001; 53(6):389-95. · 1.59 Impact Factor
  • T Shimada, K Yoshiura, A Terano
    Nippon rinsho. Japanese journal of clinical medicine 05/2001; 59 Suppl 4:60-4.

Publication Stats

2k Citations
809.99 Total Impact Points

Institutions

  • 1989–2008
    • The University of Tokyo
      • • Faculty & Graduate School of Medicine
      • • Department of Internal Medicine
      • • Division of Internal Medicine
      Tokyo, Tokyo-to, Japan
  • 1993–2006
    • Dokkyo Medical University
      • • Department of Gastroenterology (Hospital)
      • • Department of Gastroenterology
      • • Department of Surgical and Molecular Pathology
      Tochigi, Tochigi-ken, Japan
  • 1996–2001
    • Dokkyo University
      Edo, Tōkyō, Japan
  • 1997
    • California State University, Long Beach
      Long Beach, California, United States
  • 1988–1997
    • Long Beach Memorial Medical Center
      Long Beach, California, United States
  • 1990
    • Tokyo Medical University
      • Division of Radiology
      Edo, Tōkyō, Japan