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Hidetaka Matsui

Publications and source records attributed to Hidetaka Matsui.

14 recordsLinked to original sources

Direct effects of nitric oxide on histamine release from rat enterochromaffin-like cells.

The direct effects of nitric oxide (NO) on enterochromaffin-like (ECL) cells have not yet been demonstrated. In this study we investigated the direct effects of NO donors on rat ECL cells. The NO donor, NOR3 (10 and 100 microM), decreased gastrin-induced histamine release. 100 microM NOR3 increased cGMP levels and reduced gastrin-induced calcium influx. ODQ, an inhibitor of guanylate cyclase, completely blocked NOR3-induced inhibition of histamine release. These results suggest that NO inhibits gastric acid secretion via suppression of gastrin-induced histamine release through a pathway in which NO activates guanylate cyclase, in addition to increasing cGMP levels and reducing gastrin-induced calcium influx. The use of NO as a new type of gastric acid inhibitor that decreases histamine levels in the stomach would be beneficial as increased histamine levels resulting from use of a histamine H2 receptor antagonist or proton pump inhibitor have various effects on tumors and immunological functions.

Animals↗

Molecular characterization and distribution of motilin family receptors in the human gastrointestinal tract.

BACKGROUND: Motilin and ghrelin have been recognized as important endogenous regulators of gastrointestinal motor function in mammals, mediated respectively by the motilin receptor and by the closely related ghrelin receptor. The aims of this study were to explore the distribution of motilin and ghrelin receptors along the human gastrointestinal tract and to establish the molecular nature of the human motilin receptor. METHODS: Post mortem and surgical human tissue specimens with no hemorrhage, necrosis, or tumor were obtained from various parts of the gastrointestinal tract. We analyzed levels of expression of mRNA for motilin and ghrelin receptors and examined their molecular identities. Portions of some specimens were also studied by immunohistochemistry for expression of the motilin and ghrelin receptor. RESULTS: The long form of the motilin receptor, but not the short form, was expressed in all parts of the gastrointestinal tract, and expressed at higher levels in muscle than in mucosa. Motilin receptor immunoreactivity was present in muscle cells and the myenteric plexus, but not in mucosal or submucosal cells. In contrast, ghrelin receptor mRNA was expressed equally in all parts of the gastrointestinal tract, with similar levels of expression in mucosal and muscle layers. CONCLUSIONS: Both the motilin and ghrelin receptors are expressed along the human gastrointestinal tract, but they have clearly distinct distributions in regard to both level and layer. The diffuse muscle expression of the motilin receptor, at both the levels of the gene and the protein product, along the entire gastrointestinal tract makes it a useful potential target for motilide drugs for dysmotility.

Adult↗

[Usefulness of branched-chain amino acid (BCAA)-enriched nutrient mixture for nutritional treatment undergoing endoscopic treatment for esophageal varices].

We investigated the alteration of nutritional status in 144 patients who were treated for the first time with endoscopic sclerotherapy or endoscopic variceal ligation during their therapies. The serum levels of albumin, cholinesterase and total cholesterol were compared before and after treatment. The serum level of cholinesterase declined significantly. To investigate the impact of aging on the changes of nutritional status we divided all patients into two groups: (1) under 65 years, and (2) over 65 years. The decline of serum albumin of elderly patients (n=65) was significantly greater than that of younger patients (n=79). A branched-chain amino acid (BCAA)-enriched nutrient mixture for nutritional treatment significantly suppressed the decline of serum albumin in elderly patients. Nutritional treatment with a BCAA-enriched nutrient mixture should be considered during endoscopic therapy for esophageal varices, especially in elderly patients.

Adult↗

Effects of antihyperlipidemic agents on hepatic insulin sensitivity in perfused Goto-Kakizaki rat liver.

BACKGROUND: We previously reported that the Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, has hepatic insulin resistance using a perfused rat liver model. Pioglitazone, eicosapentaenoic acid (EPA), and fenofibrate are antihyperlipidemic agents and improve glucose tolerance. There have been few studies showing that these agents directly improve hepatic insulin sensitivity in type 2 diabetes mellitus. The aim of this study was to explore the effects of these agents on hepatic insulin sensitivity directly using a perfused GK rat liver model. METHODS: GK rats were treated with oral pioglitazone (6 or 10 mg/kg body weight), EPA (1 or 2 g/kg body weight), or fenofibrate (30 mg/kg body weight) for 2 weeks. Livers were perfused in situ with glucagon or with glucagon and insulin, and hepatic glucose outputs were measured. RESULTS: In the pioglitazone-treated GK rats, blood glucose levels were significantly decreased. In the pioglitazone- and EPA-treated GK rats, insulin infusion significantly attenuated hepatic glucose output stimulated by glucagon. In the fenofibrate-treated GK rats, fat deposits in the hepatocytes were decreased, and glucose output elicited by glucagon was significantly decreased compared with that in the untreated GK rats, whereas insulin infusion did not affect glucose output by glucagon. CONCLUSIONS: These findings suggest that pioglitazone and EPA may improve glucose tolerance by directly increasing hepatic insulin sensitivity, while fenofibrate may improve glucose tolerance by improving hepatic glycogen metabolism in the GK rats. We previously reported that the Goto-Kakizaki (GK) rat, an animal model of type 2 diabetes, has hepatic insulin resistance using a perfused rat liver model. Pioglitazone, eicosapentaenoic acid (EPA), and fenofibrate are antihyperlipidemic agents and improve glucose tolerance. There have been few studies showing that these agents directly improve hepatic insulin sensitivity in type 2 diabetes mellitus. The aim of this study was to explore the effects of these agents on hepatic insulin sensitivity directly using a perfused GK rat liver model.

Animals↗

Earlier recurrence of esophageal varices, following therapy, in patients with primary biliary cirrhosis (PBC) compared with non-PBC patients.

BACKGROUND: Variceal bleeding is a common, life-threatening complication of primary biliary cirrhosis (PBC). Recently, several reports have suggested that the existence of esophageal varices in patients with PBC is a significant factor in the assessment of disease prognosis. However, there have been no reports on the recurrence of esophageal varices following treatment in patients with PBC. In this study, we investigated the recurrence of esophageal varices in PBC patients and attempted to identify predictive factors for the recurrence of esophageal varices. METHODS: Between April 1993 and August 2003, 138 patients with esophageal varices who had been treated by endoscopic variceal ligation (EVL; 96 men and 42 women; age, 33-83 years; mean, 62.6 +/- 10.1 years), were enrolled in the present study. The diagnosis of esophageal varices was made by upper gastrointestinal endoscopy, and the varices were graded according to the criteria of the Japanese Research Society for Portal Hypertension. The relationship between the recurrence of esophageal varices and factors such as biochemical and hematological parameters, as well as the etiology of the liver disease, was analyzed using the Kaplan-Meier method and the multivariate Weibull regression model. RESULTS: PBC patients had an earlier recurrence of esophageal varices compared to non-PBC patients, and two factors, prothrombin time and etiology (PBC/non-PBC), were indicative of significantly earlier recurrence of esophageal varices. CONCLUSIONS: We should be extra careful in the follow-up of patients with PBC after therapy for esophageal varices.

Case-Control Studies↗

Recent clinical features of Wilson's disease with hepatic presentation.

BACKGROUND: We carried out this study to evaluate recent clinical features of Wilson's disease (WD) with hepatic presentation, especially in terms of age, degree of liver injury, and association with hepatocellular carcinoma (HCC). METHODS: Sixteen patients with hepatic manifestations were diagnosed with WD in the period 1976-2003. We divided this period into two periods, "past" and "recent". The diagnosis was based on the presence of Kayser-Fleisher rings, low serum copper levels, low serum ceruloplasmin levels, increased urinary copper concentrations before or after D-penicillamine challenge, and increased hepatic copper concentrations. This retrospective study was done at Ehime University Hospital. RESULTS: Four patients, including a pair of siblings, had a family history of WD. Four patients had parental consanguinity. There were 6 patients aged over 40 years in the recent period, whereas no patients in the past period were over 40. Four patients had neurological manifestations. Ten patients had liver cirrhosis and 5 had chronic hepatitis. Two had fatty liver without obesity. All patients in the past period had liver cirrhosis. Three patients with liver cirrhosis were found to have HCC during the follow up. All patients were treated with either D-penicillamine or trientine chloride, or both. However, four patients had to discontinue these agents due to the side effects. CONCLUSIONS: Recently, the number of patients diagnosed with WD has been increasing, not only in terms of those with classical-type WD but also in terms of elderly patients or patients with non-cirrhotic liver injury such as fatty liver and chronic hepatitis. The various clinical features of WD should be recognized and particular attention should focus on HCC as a complication.

Adolescent↗

Mechanism of action of low recurrence of gastritis caused by Helicobacter pylori with the type II urease B gene.

BACKGROUND: Low recurrence of gastritis is seen in patients infected with Helicobacter pylori carrying the type II urease B gene, compared with H. pylori carrying types I and III. The underlying mechanism has been studied in terms of the urease activity and interleukin (IL)-8 production capacity of different strains of H. pylori. MATERIALS AND METHODS: Forty-five patients infected with different strains of H. pylori (type I; 15, type II; 15 and type III; 15) were enrolled in the study. H. pylori was isolated from gastric mucosa and cultured in the presence of urea at pH 5.5 to evaluate urease activity. The capacity of different strains of H. pylori to induce IL-8 mRNA and IL-8 from a human gastric cancer cell line and human peripheral blood mononuclear cells was evaluated. RESULTS: The urease activity of type II H. pylori[523 +/- 228 micro g of ammonia/dl/10(8) colony-forming units (CFU)/ml] was significantly lower than that of type I (1355 +/- 1369 micro g of ammonia/dl/10(8) CFU/ml) and type III (1442 +/- 2229 micro g of ammonia/dl/10(8) CFU/ml) (p <.05). Gastric cancer cells cocultured with type II H. pylori produced lower levels of IL-8 mRNA compared with type I and type III H. pylori. The levels of IL-8 were also significantly lower in cultures induced by type II H. pylori compared with those induced by type I and type III H. pylori. Peripheral blood mononuclear cells also produced lower levels of IL-8 when cocultured with type II compared with type I H. pylori. CONCLUSIONS: These results indicate that both the lower level of urease activity and the low IL-8-inducing capacity of type II H. pylori might underlie the lower recurrence rate of gastritis caused by type II H. pylori.

Antigens, Bacterial↗

Direct effects of proton pump inhibitors on histamine release from rat enterochromaffin-like cells.

Enterochromaffin-like (ECL) cells play a central role in the regulation of gastric acid secretion. Previous studies have shown that proton pump inhibitors accelerate histamine release from ECL cells through the effects of gastrin. However, direct effects of proton pump inhibitors on ECL cells have not been demonstrated to date because the indirect effects of gastrin are difficult to suppress. We investigated the direct effects of proton pump inhibitors medication on ECL cells using an elutriation system. ECL cells were stimulated with gastrin or rabeprazole, and histamine release from ECL cells was measured. Rabeprazole increased histamine release through a pathway that differed from that of gastrin. The histamine increase was likely due to an acceleration of vesicular monoamine transporter 2 (VMAT2). Rabeprazole increased histamine release from ECL cells directly via VMAT2, but did not affect the total amount of histamine in the cells. The results suggest that patients receiving proton pump inhibitors for extended periods must be monitored extensively because gastric tumor proliferation may be promoted by increased histamine release from ECL cells.

2-Pyridinylmethylsulfinylbenzimidazoles↗

Esophagogastric varices as a prognostic factor for the determination of clinical stage in patients with primary biliary cirrhosis.

BACKGROUND: Primary biliary cirrhosis (PBC) is usually classified as either asymptomatic PBC (a-PBC) or symptomatic PBC (s-PBC). Although the proportion of a-PBC versus s-PBC patients has been consistently increasing, it is not clear whether the present criteria for the staging of PBC are optimal or not. We investigated the clinical stage of PBC patients from the standpoint of esophagogastric varices (EGV). METHODS: One hundred and nine PBC patients were enrolled in this retrospective study. We investigated the clinical features of PBC based on laboratory data, histological stage, symptoms, and existence of EGV. In addition, the clinical course and prognosis in patients who were periodically followed up were also studied. RESULTS: (1) EGV was detected in a-PBC patients, and there was no difference in the grade of EGV between a-PBC and s-PBC patients. (2) a-PBC patients with EGV had more liver damage than those without EGV, and a-PBC patients with EGV had a poorer prognosis than those without EGV. (3) Three of 11 patients who progressed from a-PBC to s-PBC within 3 years had EGV. (4) One of 3 a-PBC patients with EGV had progressed to s-PBC at 3-year follow-up. CONCLUSIONS: These results indicate that EGV is one of the most important factors for evaluating PBC. Therefore, we would like to propose that a-PBC patients with EGV should either be included in the presently defined s-PBC class, or that new prognostic classes of PBC be created that include EGV as a prognostic factor.

Adult↗

Depletion and decreased function of antigen-presenting dendritic cells caused by lymphocytapheresis in ulcerative colitis.

PURPOSE: The therapeutic efficacy of lymphocytapheresis in autoimmune diseases is presumed to be caused by depletion of activated lymphocytes. However, nothing is known about the inducer of activated lymphocytes, the antigen-presenting dendritic cells, during lymphocytapheresis. BASIC PROCEDURES: Six sessions of lymphocytapheresis were done in five patients with ulcerative colitis. Dendritic cells were enriched from the buffy coat of depleted lymphocytes and also from the peripheral blood. The phenotype and function of dendritic cells were studied by dual-color flow cytometry and in allogenic mixed leukocyte reaction, respectively. The serum levels of inflammatory cytokines (interleukin-1alpha 6, 8, 10, and 12 and tumor necrosis factor-alpha and beta) were measured before and after lymphocytapheresis in all cases. MAIN FINDINGS: Lymphocytapheresis was safe and caused clinical, endoscopic or histologic improvements in all patients with ulcerative colitis. Many CD83-positive mature dendritic cells were found in the buffy coats after each session of lymphocytapheresis. The function of dendritic cells, the frequencies of CD83-positive dendritic cells and the levels of interleukin-6 and interleukin-8 were down regulated in all patients with ulcerative colitis after lymphocytapheresis compared with their levels before lymphocytapheresis. CONCLUSIONS: Depletion and down regulation of the function of dendritic cells and diminished levels of inflammatory cytokines caused by lymphocytapheresis may contribute to the therapeutic efficacy of lymphocytapheresis.

Adolescent↗

Antigen-presenting dendritic cells in ulcerative colitis.

BACKGROUND: Antigen-presenting dendritic cells are the inducers and regulators of immune responses. Here, we have discussed the phenotype and function of dendritic cells in situ and their alteration during lymphocytapheresis in patients with ulcerative colitis. METHODS: Dendritic cells were enriched from the peripheral blood mononuclear cells by culturing with granulocyte-macrophage colony-stimulating factors and interleukin 4 for 8 days. The function of dendritic cells was evaluated in an allogenic mixed leukocyte reaction. Flow cytometry was employed to study the phenotype of dendritic cells. Lymphocytapheresis was done by a continuous flow centrifugation technique using a CS-3000 separator. Immunohistochemical methodology was employed to detect dendritic cells at the colonic mucosa. RESULTS: Peripheral blood dendritic cells had increased functional capacity, and these cells were matured and activated compared to dendritic cells from normal controls. CD83-positive activated and mature dendritic cells were found at the colonic mucosa from patients with ulcerative colitis. Lymphocytapheresis induced decreased function of peripheral blood dendritic cells in patients with ulcerative colitis. Also, the levels of inflammatory cytokines were reduced by lymphocytapheresis. CONCLUSIONS: Increased function of dendritic cells may be related to the inflammatory mucosal milieu found in patients with ulcerative colitis. Depletion of dendritic cells during lymphocytapheresis may downregulate the exacerbated immune response in patients with ulcerative colitis.

Antigen-Presenting Cells↗

Clinical characteristics of autoimmune hepatitis with histological features of acute hepatitis.

The number of patients with autoimmune hepatitis with histological features of acute hepatitis (AIH-AH) has been increasing recently. Here, the clinical features of patients with AIH-AH have been compared with those of patients with AIH with histological findings of chronic hepatitis (AIH-CH) and liver cirrhosis (AIH-LC). The levels of total serum bilirubin (P<0.05) and serum transaminases (P<0.05) were significantly higher in patients with AIH-AH than in patients with AIH-CH and AIH-LC. However, the serum levels of gamma-globulin (P<0.05) and immunoglobulin G (P<0.05) were significantly lower in AIH-AH than in patients with AIH-CH and AIH-LC. The aggregate score according to the criteria of the International Autoimmune Hepatitis Group in 1999 was also significantly lower in AIH-AH patients than in patients with AIH-CH and AIH-LC (P<0.05). Eleven patients with AIH-AH were treated with corticosteroids, however, the clinical response was insignificant in three patients. In summary, it is difficult to diagnose of patients with AIH-AH using the criteria of the International AIH scoring system. We wish that this scoring system would be modified in the near future.

Journal Article↗