[Peptic ulcer: current status and perspectives].
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Animals↗
Biomedical subjects
Akira Terano
Publications and source records attributed to Akira Terano.
Effect of central thyrotropin-releasing hormone on pancreatic blood flow in rats.
Central neuropeptides play a role in physiological regulation through the autonomic nervous system. Thyrotropin-releasing hormone (TRH) is a neuropeptide distributed throughout the central nervous system and acts as a neurotransmitter to regulate gastric and hepatic functions through vagal-cholinergic pathways. In this study, the central effect of TRH on pancreatic blood flow was investigated in urethane-anesthetized rats. Pancreatic blood flow was determined by laser Doppler flowmetery. After measurement of basal blood flow, a stable TRH analog, RX 77368 (1-50 ng) or saline was injected intracisternally. Pancreatic blood flow was observed for 120 min thereafter. In some experiments, pretreatment with atropine methyl nitrate (0.15 mg/kg, i.p.), NG-nitro-L-arginine-methyl ester (10 mg/kg, i.v.), or 6-hydroxydopamine (6-OHDA;180 mg/kg, i.p.), or subdiaphragmatic vagotomy was performed. Intracisternal injection of TRH analog dose-dependently increased pancreatic blood flow with a peak response occurring 30 min after injection. The stimulatory effect of TRH analog on pancreatic blood flow was blocked by vagotomy, atropine, and NG-nitro-L-arginine-methyl ester, but not by 6-hydroxydopamine. Intravenous administration of the TRH analog did not influence pancreatic blood flow in the same animal model. These results indicate that TRH acts in the central nervous system to stimulate pancreatic blood flow through vagal-cholinergic and nitric oxide-dependent pathways.
Animals↗
Identification and characterization of taxilin isoforms.
The syntaxin family is implicated in intracellular vesicle traffic. We have recently identified taxilin, a novel syntaxin-binding protein, which has a long coiled-coil region in its C-terminal half. A database search has revealed the presence of two other molecules having a long coiled-coil region homologous to that of taxilin in mammals. Then, we here attempted to isolate and characterize the two molecules. Both the two molecules stoichiometrically interacted with several syntaxin family members. Then, we renamed original taxilin alpha-taxilin and named the two molecules beta- and gamma-taxilins, respectively. Beta-taxilin was a human homologue of chicken MDP77. Gamma-taxilin was an uncharacterized protein and Northern blot analysis revealed that gamma-taxilin was ubiquitously expressed. Beta- and gamma-taxilins preferentially interacted with syntaxin-1a and -4, respectively. The taxilin family members mutually interacted with the syntaxin family members. These results indicate that there is the taxilin family composed of at least three members in mammals.
Animals↗
Intraportal nicotine infusion in rats decreases hepatic blood flow through endothelin-1 and both endothelin A and endothelin B receptors.
Smoking has been demonstrated to aggravate liver injury. Nicotine, a major pharmacological component of tobacco smoke, affects a multitude of functions. Smoking and nicotine induce synthesis of endothelin (ET)-1. The effect of intraportal infusion of nicotine on hepatic circulation and an involvement of ET-1 and ET receptor in the action of nicotine were investigated in rats. Nicotine (0-100 microg/kg/h) was infused into the portal vein of urethane-anesthetized rats, and changes of hepatic blood flow were evaluated. Intraportal infusion of nicotine dose-dependently decreased hepatic blood flow and increased portal pressure without any alteration of heart rate or arterial blood pressure. This action of intraportal nicotine was completely abolished by pretreatment of ET-1 antibody. Either BQ485 (ET(A) receptor antagonist) or BQ788 (ET(B) receptor antagonist) partially reversed the effect of nicotine, and combination of BQ788 and BQ485 completely abolished it. These findings suggest that nicotine inhibits hepatic circulation through ET-1, and ET(A) and ET(B) receptor.
Animals↗
PPARgamma mediates NSAIDs-induced upregulation of TFF2 expression in gastric epithelial cells.
Trefoil factor family (TFF) is a group of peptides that play critical roles in maintaining gastric mucosal integrity. In real-time quantitative reverse transcription-polymerase chain reaction (RT-PCR) and reporter gene assays, we show that indomethacin and aspirin upregulate TFF2 expression in MKN45 gastric cells. These drugs also activated peroxisome proliferator-activated receptor gamma (PPARgamma) at concentration ranges that increase TFF2 expression, and upregulated TFF2 expression was suppressed by GW9662, a specific inhibitor of PPARgamma. These results suggest that indomethacin and aspirin upregulate gastric expression of TFF2 through activation of PPARgamma. This mechanism may be important in reducing the extent of gastric mucosal injury caused by the administration of non-steroidal anti-inflammatory drugs (NSAIDs).
Anilides↗
Vitamin E therapy in patients with NASH.
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Alanine Transaminase↗
Transforming growth factor-beta-induced stimulation of formation of collagen fiber network and anti-fibrotic effect of taurine in an in vitro model of hepatic fibrosis.
The cell strain M, which was established from normal rat liver cells, is characterized by the active formation of a collagen fiber network. In this study, we investigated the characterization of M cells and evaluated the anti-fibrogenic effects of taurine using this culture system. M cells expressed cytokeratin (CK)8, CK18, vimentin, and alpha-smooth muscle actin, whereas expression of CK-19 or desmin was not detected. Also, M cells expressed transforming growth factor (TGF)-beta1, -beta2, and TGF-beta type I and II receptors, and treatment with TGF-beta1 (1ng/ml) for 6 days markedly stimulated the formation of a collagen fiber network and expression of procollagen alpha1(I) mRNA. When M cells were treated with various concentrations of taurine (10-50mM), network formation and procollagen alpha1(I) expression were significantly suppressed in a dose dependent manner. Additionally, even in the presence of TGF-beta1, taurine treatment effectively reduced the formation of a collagen fiber network. These results suggest that M cells exhibit features of not only hepatocytes but also myofibroblasts, and TGF-beta1 plays an important role in the formation of collagen fiber networks in this culture system. Additionally, this M cell culture system is appropriate for use as an in vitro model of hepatic fibrosis in the evaluation of the anti-fibrogenic effects of various agents.
Journal Article↗
Development of quantitative neuropsychological tests for diagnosis of subclinical hepatic encephalopathy in liver cirrhosis patients and establishment of diagnostic criteria-multicenter collaborative study in Japanese.
At present, there are no generally accepted diagnostic criteria or methods for subclinical hepatic encephalopathy (SHE) associated with liver cirrhosis. We therefore developed an easily conducted computer-aided quantitative neuropsychiatric function test system for use in routine medical practice. We established normal values in healthy Japanese subjects and determined differences between healthy persons and liver cirrhosis patients without clinical encephalopathy in a multi-center clinical trial. The test system consists of eight tests: number connection tests A and B, a figure position test, a digit symbol test, a block design test, and reaction time tests A, B and C. The test results were affected by age, but not by gender or facility. No learning effect was noted. The results were therefore reported by 5-year quartile ranges and differences were evaluated between 542 healthy subjects and 292 cirrhotic patients. When the cut-off value was set at the 10th/90th percentile of the results in healthy subjects, the results of each of the 8 tests were abnormal in about 25% of cirrhotic patients, and at least 1 of the 8 tests gave values greater than the 10th/90th percentile cut-off value in 58.2% of the 292 liver cirrhosis patients. SHE patients were thought to be included in these 58.2% of patients. The developed test makes it possible to quantitatively assess neuropsychiatric function, and the results obtained can be used as a basis for the diagnosis of SHE.
Journal Article↗
Photodynamic therapy of superficial esophageal cancer with a transparent hood.
BACKGROUND: To improve the effectiveness of photodynamic therapy, the further development of endoscopic devices is essential. For photodynamic therapy of superficial esophageal cancer, a transparent hood was used to obtain precise laser irradiation. METHODS: The transparent hood was attached to the tip of an upper endoscope. Forty-eight hours after the injection of porfimer sodium, cancerous lesions were irradiated with an excimer-dye laser (4 mJ, 80 Hz). Twenty-four hours later, additional irradiation was applied to lesions when the response to the initial irradiation appeared insufficient. Fifteen neoplastic lesions in 7 patients were treated. RESULTS: The initial size of the lesions ranged from 5 to 30 mm in diameter. Histopathologically, there were 9 squamous-cell carcinomas and 6 high-grade squamous dysplastic lesions. All treated lesions disappeared after the first or the second laser irradiation (total energy range 39.1-193.5 J/cm(2)). During follow-up (range 4-51 months), there was no recurrence of the initial lesion in any patient. There was no severe photodynamic therapy related complication. CONCLUSIONS: Photodynamic therapy with a transparent hood is an acceptable option for the treatment of superficial esophageal cancer.
Aged↗
Evaluation of esophageal varices using contrast-enhanced coded harmonic ultrasonography.
AIM: To investigate if esophageal varices can be evaluated using external contrast-enhanced ultrasonography with Levovist and coded harmonic angio (CHA). METHODS: Subjects were six healthy adult volunteers and 23 patients with liver cirrhosis. After identification of the lower esophagus under B-mode scanning, 300 mg/mL of Levovist was intravenously injected into the cubital vein at a rate of 1 mL/s under observation by CHA-mode scanning. Approximately 30 s after intravenous administration, interval-delay scanning was performed every second to visualize the area around the lower esophageal lumen. The degree of ultrasonographic enhancement was assessed as either no enhancement (negative); linear enhancement along the esophageal wall (weak) or full enhancement of the esophageal lumen (strong). Endoscopic evaluation of esophageal varices was also performed. RESULTS: The CHA enhancement around the lower esophageal lumen was identified in 21 of the 23 patients. Of these 21 patients, endoscopic assessments of varices were as follows: F0 in four patients, F1 in seven patients, F2 in three patients, and F3 in seven patients. Nine patients were red color sign (RCS)-positive. Regarding the relationship between ultrasonographic enhancement and endoscopic assessment, enhancement was identified as negative in all four F0 patients, negative in three and weak in three and strong in one of the seven F1 patients, weak in one and strong in two of the three F2 patients, and weak in two and strong in five of the seven F3 patients, respectively. Furthermore, of the nine RCS-positive patients, enhancement was recognized as strong in seven and weak in two patients. Ultrasonographic enhancement was identified as negative in all six healthy volunteers. CONCLUSIONS: By performing contrast-enhanced CHA ultrasonography using Levovist, ultrasonographic enhancement was detectable in all patients with varices categorized as F2 or above. Because the present method is easy to perform and causes less pain to patients compared to endoscopy, it is useful for following and assessing esophageal varices in patients with liver cirrhosis.
Aged↗
[Clinical characteristics of gastric and duodenal ulcer].
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Humans↗
[For the prevention of medical malpractice--the current status and the proposal].
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Clinical Competence↗
[Recent view of gastro-esophageal reflux disease according to the guideline for gastric ulcer treatment].
The guideline for gastric ulcer treatment in Japan recommends eradication of Helicobacter pylori (H. pylori) for the first choice. Recently, it is well known that some patients develop gastro-esophageal reflux disease (GERD) after successful eradication. H. pylori infection may play a protective role against GERD by impairing gastric acid secretion. Acid secretion is influenced by the distribution of gastritis in the stomach. Antrum-predominant gastritis is associated with gastric hypersecretion. Patients with corpus-predominant gastritis have decreased acid secretion. The latter is common in Japan and at high risk of GERD after eradication. To arise GERD, both acid secretion and reflux of acid caused by hiatus hernia or gastro-esophageal dysmotility are needed. Although most of GERD developed after eradication are mild, severe GERD are also experienced at times. Recent view of GERD and H. pylori infection is described.
Esophageal Motility Disorders↗
[Present status and prospects of wireless capsule endoscopy].
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Endoscopes, Gastrointestinal↗
Interaction of taxilin with syntaxin which does not form the SNARE complex.
Taxilin is novel binding partner of the syntaxin family, which is implicated in intracellular vesicle traffic. However, precise binding properties of taxilin to the syntaxin family remain to be clarified. Then, we here further investigated the interaction of taxilin with the syntaxin family by use of recombinant taxilins. Syntaxin-1a, -3, and -4 bound to taxilin in a dose-dependent and saturable manners. The concentrations of syntaxin-1a, -3, and -4 giving a half-maximal binding to taxilin were about 1.5, 3.0, and 1.0microM, respectively. The interaction of taxilin with syntaxin-1a was inhibited by SNAP-25 or Munc18 in a dose-dependent manner. When recombinant taxilin was incubated with the extract from the rat brain crude membrane fraction, recombinant taxilin bound to syntaxin-1s free of at least VAMP2, SNAP-25, and Munc18. These results suggest that taxilin interacts with the syntaxin family which does not form at least the SNARE complex.
Animals↗
Involvement of calcitonin gene-related peptide and capsaicin-sensitive afferents in central thyrotropin-releasing hormone-induced hepatic cytoprotection.
The involvement of capsaicin-sensitive afferent neurons and calcitonin gene-related peptide (CGRP) in central thyrotropin-releasing hormone (TRH)-induced hepatic cytoprotection was investigated in rats. Both systemic capsaicin pretreatment and intravenous administration of CGRP receptor antagonist, human CGRP-(8-37), completely abolished the protective effect of intracisternal TRH analog (RX-77368; p-Glu-His-(3,3'-dimethyl)-Pro-NH2, 5 ng) against carbon tetrachloride (CCl4)-induced acute liver injury, assessed by serum alanin aminotransferase levels and histological changes. These data demonstrate the involvement of capsaicin-sensitive afferent neurons and CGRP in central TRH-induced hepatic cytoprotection.
Animals↗
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↗
Extranodal diffuse follicular center lymphoma mimicking mantle cell lymphoma of the intestine.
We report a case of diffuse follicular center lymphoma (FCL), which is a morphological variant of follicular lymphoma, resembling multiple lymphomatous polyposis (mantle cell lymphoma of the intestine). The patient was a 48-year-old Japanese man who was found, by colonoscopy, to have numerous small polypoid lesions along the entire large intestine. Abdominal computed tomography revealed hepatosplenomegaly and enlargement of multiple mesenteric lymph nodes. Histologically, the lesion was characterized by diffuse proliferation of small- to medium-sized lymphocytes with cleaved nuclei in the mucosa and submucosa. Immunohistochemical studies showed that the tumor cells were CD20+, CD10+, BCL-2+, CD5-, surface IgM-, and cyclin D1-. Moreover, a cytogenetic study showed a translocation at (14;18)(q32;q21). Finally, this case was diagnosed as diffuse FCL, although the tumor was mimicking mantle cell lymphoma.
Chromosomes, Human, Pair 14↗