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Akira Terano

Publications and source records attributed to Akira Terano.

At least 19 recordsLinked to original sources
PubMed2003

Central injection of astressin inhibits carbon tetrachloride-induced acute liver injury in rats.

The effect of intracisternal astressin, a specific and potent corticotropin-releasing factor (CRF)(1) and CRF(2) receptor antagonist on carbon tetrachloride (CCl(4))-induced acute liver injury was investigated in rats. Intracisternal astressin inhibited the elevation of serum alanine aminotransferase level induced by CCl(4). Intracisternal astressin also reduced CCl(4)-induced liver histological changes. The protective effect of central astressin on CCl(4)-induced liver damage was abolished by sympathectomy but not by hepatic branch vagotomy. These findings demonstrate that astressin acts in the central nervous system to induce hepatic cytoprotection, possibly through the sympathetic pathways in rats. These results further establish a role of endogenous CRF in the brain in hepatic pathophysiological regulation.

Alanine Transaminase↗
PubMed2003

Evaluation of cell proliferation and apoptosis in Helicobacter pylori gastritis using an image analysis processor.

BACKGROUND: Infection of the gastric mucosa by helicobacter pylori is primarily responsible for gastritis, gastric ulcer, adenocarcinoma, and lymphoproliferative disorders. H. pylori appears to accelerate apoptosis and the proliferation of the gastric epithelium directly or indirectly. To precisely assess the proliferative and apoptotic profile of .H pylori-infected gastric mucosa, a quantitative imaging system is now required. METHODS: Fifty-two patients with H. pylori gastritis were the subjects of the study. Biopsy materials were taken from at least two sites (usually three to five sites) including the antrum and corpus. The grade of gastritis was evaluated by the updated Sydney System. The proliferative and apoptotic profile was examined by Ki-67 immunohistochemistry and by a terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling method. In addition, Ki-67-positive cells were quantitated by an image processor for analytical pathology (IPAP) system. RESULTS: H. pylori density and polymorphonuclear neutrophil activity were significantly decreased after H. pylori eradication ( P< 0.0001). Chronic inflammation (P< 0.0001) and lymphoid follicle numbers ( P < 0.0005) were also significantly decreased after the eradication. Glandular atrophy and intestinal metaplasia were slightly decreased after eradication, but the decrease did not reach the significant level. the Ki-67 labeling index was significantly decreased after the eradication P< 0.0001). The apoptosis index was also decreased after the eradication, but this decrease did not reach the significant level ( P = 0.06). CONCLUSION: our data suggest that the activation of proliferative cells and induction of apoptosis in the gastric mucosa is a response to H. pylori-induced mucosal damage. Moreover, IPAP may be a useful technology for evaluating the results of immunohistochemistry, and it could provide quantitative and reliable data for studying H. pylori gastritis.

Adult↗
PubMed2003

Protective effect of central thyrotropin-releasing hormone on carbon tetrachloride-induced acute hepatocellular necrosis in rats.

BACKGROUND/AIMS: Thyrotropin-releasing hormone (TRH) acts in the brain to stimulate hepatic proliferation and blood flow through vagal-muscarinic and prostaglandin-mediated pathways. Hepatic blood flow and prostaglandins are well recognized as cytoprotective factors for liver damage, and central TRH is known to play a role in gastric cytoprotection. The effect of central TRH on carbon tetrachloride (CCl(4))-induced acute hepatocellular necrosis was investigated in rats. METHODS: Male fasted rats were injected with either TRH analog, RX 77368 (1-10 ng), or vehicle intracisternally, and CCl(4) (2.0 ml/kg) was injected subcutaneously 60 min later. Acute hepatocellular necrosis was assessed by serum hepatic enzymes and histological changes 24 h after CCl(4). RESULTS: Intracisternal TRH dose-dependently inhibited elevation of serum alanine aminotransferase level induced by CCl(4). Intracisternal TRH reduced CCl(4)-induced hepatic histological changes. The cytoprotective effect of central TRH on CCl(4)-induced acute hepatocellular necrosis was abolished by hepatic branch vagotomy, atropine, indomethacin and N(G)-nitro-L-arginine methyl ester, but not by 6-hydroxydopamine. Intravenous TRH did not influence CCl(4)-induced acute hepatocellular necrosis. CONCLUSIONS: These results suggest that the cytoprotective effect of central TRH on acute hepatocellular necrosis is mediated through vagal-muscarinic, and prostaglandin- and nitric oxide-dependent pathways.

Acute Disease↗
PubMed2003

Taxilin; a novel syntaxin-binding protein that is involved in Ca2+-dependent exocytosis in neuroendocrine cells.

BACKGROUND: The syntaxin family is a central coordinator and participates in multiple protein-protein interactions in the soluble N-ethyl maleimide-sensitive factor attachment protein receptor machinery, which is involved in intracellular vesicle traffic. However, the molecular mechanism by which the syntaxin family regulates intracellular vesicle transport is not well known. RESULTS: We have identified and purified a novel binding partner of syntaxin-3 from rat lung, and isolated and sequenced the cDNA of its human homologue from a human brain cDNA library. The cDNA had an open reading frame encoding a protein of 546 amino acids with a calculated Mr of 61,890. We tentatively referred to this protein as taxilin. A structural analysis of taxilin revealed the existence of an extraordinarily long coiled-coil domain in its C-terminal half. Syntaxin-1a and -4, as well as syntaxin-3 interacted with taxilin, but syntaxin-7 or -8 did not. Northern blot analysis showed that taxilin was ubiquitously expressed. Over-expression of full-length taxilin inhibited Ca2+-dependent exocytosis in PC12 cells. CONCLUSIONS: These results indicate that taxilin is a novel binding partner of several syntaxin family members and suggest that taxilin is involved in Ca2+-dependent exocytosis in neuroendocrine cells.

Animals↗
PubMed2003

Lafutidine increases hepatic blood flow via potentiating the action of central thyrotropin-releasing hormone in rats.

BACKGROUND: Lafutidine, (+/-)-2-(furfurylsulfinyl)-N-[4-[4-(piperidinomethyl)-2-pyridyl]oxy-(Z)-2 butenyl]acetamide, is a newly synthesized histamine H2 receptor antagonist and possesses a cytoprotective efficacy, which comprises mucin biosynthesis and stimulation of gastric blood flow mediated through capsaicin-sensitive sensory neurons and endogenous calcitonin gene-related peptide (CGRP). In the present study, an effect of lafutidine on hepatic blood flow was investigated in rats that received an intracisternal injection of a subthreshold dose of thyrotropin-releasing hormone (TRH) analog, RX 77368. METHODS: Change in hepatic blood flow was determined by laser Doppler flowmetry. Male Wistar rats were anesthetized with urethane (1.5 g/kg, i.p.), and positioned on a stereotaxic apparatus. An abdominal incision was made, and a probe of laser Doppler flowmeter was placed on the surface of the liver. After a 60-min stabilization, basal hepatic blood flow was measured for 30 min, and lafutidine (0.5, 1, 3, 5 or 10 mg/kg) or vehicle was injected into the portal vein and a subthreshold dose (1.5 ng) of RX 77368 was injected intracisternally. Hepatic blood flow was monitored for 120 min postinjection. To investigate a role of capsaicin-sensitive sensory neurons and endogenous CGRP, systemic capsaicin treatment (125 mg/kg, s.c., 10-14 days before) and intravenous infusion of a CGRP receptor antagonist, human CGRP-(8-37) (15 micro g/kg as a bolus, followed by infusion at 3 micro g/kg/h) were performed, respectively. RESULTS: Intracisternal injection of RX 77368 (1.5 ng) or intraportal lafutidine (10 mg/kg) by itself did not affect hepatic blood flow, but co-injection of intracisternal RX 77368 (1.5 ng) and intraportal lafutidine (5 mg/kg) increased it with peak response at 30 min postinjection. The effect of lafutidine on hepatic blood flow in rats given RX 77368 was dose-related over the range 1-5 mg/kg. By contrast, intracisternal injection of RX 77368 (1.5 ng) did not change hepatic blood flow in rats injected with another histamine H2 receptor antagonist, famotidine (5 mg/kg), intraportally. The stimulatory effect of co-injection of TRH analog and lafutidine was abolished by systemic capsaicin-treatment and CGRP antagonist. CONCLUSION: These data suggest that lafutidine increases hepatic blood flow by sensitizing the liver to the action of central TRH via both capsaicin-sensitive sensory neurons and endogenous CGRP in urethane-anesthetized rats.

Acetamides↗
PubMed2003

Identification of genes differentially expressed in a newly isolated human metastasizing esophageal cancer cell line, T.Tn-AT1, by cDNA microarray.

We isolated a metastasizing human esophageal squamous cell carcinoma (SCC) cell line, T.Tn-AT1, from a parental non-metastasizing cell line, T.Tn, by in vitro selection and by use of a nude mouse orthotopic inoculation model. Then, we compared the expression profiles of 9206 genes in T.Tn-AT1 and T.Tn by cDNA microarray analysis. The gene expression profiles of T.Tn and T.Tn-AT1 were very similar, and only 34 genes showed more than 3-fold differential expression. Among the 34 genes, 29 genes were down-regulated and only 5 genes were up-regulated in T.Tn-AT1 cells. Subsequently, we confirmed the expression levels of 14 of the 34 genes in T.Tn and T.Tn-AT1 cells by means of reverse transcription-polymerase chain reaction. The expression of 8 genes (KAL1, HPGD, NDN, REG1A, CXCR4, SPOCK, DIAPH2 and AIF1) was down-regulated and that of one gene (VNN2) was up-regulated in T.Tn-AT1 cells. These 9 genes encoded proteins associated with metastatic processes, such as adhesion, migration, inflammation, proliferation, and differentiation. Thus, these genes might regulate the metastasis of esophageal SCC, and could be predictive markers for lymph node metastasis of esophageal SCC.

Carcinoma, Squamous Cell↗
PubMed2003

[Guidelines in the management of Helicobacter pylori infection in Japan--in comparison with the guidelines published in other countries].

Helicobacter pylori(H. pylori) is a causative agent for chronic gastritis and is an important risk factor for peptic ulcers, gastric carcinomas, and gastric MALT lymphomas. In 2000, the Japanese Society for Helicobacter Research published a guideline on the diagnosis and treatment of H. pylori infection for physicians in routine medical practice. In this guideline, H. pylori eradication therapy is recommended in gastric or duodenal ulcer patients. H. pylori eradication is also recommended in gastric MALT lymphoma patients but the guideline says it should be done at specialist institutions. Considering the high prevalence of gastric carcinomas in Japan. H. pylori eradication for the prevention of gastric carcinomas should be discussed urgently.

Europe↗
PubMed2002

Serum and tissue PIVKA-II expression reflect the biological malignant potential of small hepatocellular carcinoma.

A sensitive method for measuring the serum level of protein-induced by vitamin K absence or antagonist II (PIVKA-II) has become so widely available that it is now used for the clinical diagnosis of small hepatocellular carcinoma (HCC). It is known that serum PIVKA-II can be a prognostic indicator for HCC, but there have been no detailed investigations concerning the tissue expression of PIVKA-II. The present study assessed the relationship between serum or tissue PIVKA-II and the biological malignant potential of HCC. The subjects were 25 patients with histologically confirmed HCC, that were solitary and 3 cm or less in diameter. Tissue PIVKA-II was detected by immunostaining using MU-3 as the primary antibody. The biological malignant potential of the tumors was evaluated on the basis of the Ki-67 labeling index of HCC cells and the tumor arterial vascularity assesed by angiography and CO(2) enhanced ultrasonography. The recurrence-free period after treatment was also evaluated. Among the 25 patients, eight were positive for tissue PIVKA-II. Serum PIVKA-II levels were significantly higher in the tissue PIVKA-II-positive patients compared with the negative patients, but serum and tissue PIVKA-II expressions were not consistently parallel. Tumor cell proliferation was closely correlated with the tissue PIVKA-II expression, while the recurrence-free period was correlated with the serum PIVKA-II level. Tumor arterial vascularity showed a strong correlation with the expression of both serum and tissue PIVKA-II. In conclusion, serum and tissue PIVKA-II expression reflect the biological malignant potential of HCC and thus may be useful indicators for the prognosis of small HCC.

Journal Article↗
PubMed2002

Involvement of endogenous CRF in carbon tetrachloride-induced acute liver injury in rats.

Central neuropeptides play important roles in many physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Central injection of corticotropin-releasing factor (CRF) aggravates carbon tetrachloride (CCl4)-induced acute liver injury through the sympathetic nervous pathway in rats. However, still nothing is known about a role of endogenous neuropeptides in the brain in hepatic pathophysiological regulations. Involvement of endogenous CRF in the brain in CCl4-induced acute liver injury was investigated by centrally injecting a CRF receptor antagonist in rats. Male fasted Wistar rats were injected with CRF receptor antagonist alpha-helical CRF-(9-41) (0.125-5 microg) intracisternally just before and 6 h after CCl4 (2 ml/kg) administration, and blood samples were obtained before and 24 h after CCl4 injection for measurement of hepatic enzymes. The liver sample was removed 24 h after CCl4 injection, and histological changes were examined. Intracisternal alpha-helical CRF-(9-41) dose dependently (0.25-2 microg) reduced the elevation of alanine aminotransferase and aspartate aminotransferase levels induced by CCl4. Intracisternal alpha-helical CRF-(9-41) reduced CCl4-induced liver histological changes, such as centrilobular necrosis. The effect of central CRF receptor antagonist on CCl4-induced liver injury was abolished by sympathectomy and 6-hydroxydopamine pretreatment but not by hepatic branch vagotomy or atropine pretreatment. These findings suggest the regulatory role of endogenous CRF in the brain in experimental liver injury in rats.

Acute Disease↗
PubMed2002

Diffuse nodular lymphoid hyperplasia of the large bowel without hypogammaglobulinemia or malabsorption syndrome: a case report and literature review.

Diffuse nodular lymphoid hyperplasia (DNLH) of the intestine is an extremely rare lymphoproliferative disorder occasionally associated with non-Hodgkin lymphomas. We report an unusual case of DNLH of the entire colon, which resembled malignant lymphoma (particularly low-grade B-cell lymphoma) both on clinical and pathologic grounds. The patient was a 62-year-old Japanese woman who was found to have multiple polypoid lesions along the entire large intestine by colonoscopy. Abdominal computed tomography revealed hepatosplenomegaly and multiple mesenteric lymphadenopathy. Histologically, the lesion was characterized by numerous lymphoid follicles with active germinal centers and a diffuse infiltrate of lymphoid cells in the mucosa and submucosa. The present case appears to be an essentially benign condition bearing a resemblance, both clinically and histologically, to malignant lymphoma, and from which it can be distinguished by use of immunohistochemical or molecular analysis.

Agammaglobulinemia↗
PubMed2002

[Gastric ulcer].

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Age Factors↗