Biomedical subjects

Motowo Mizuno

Publications and source records attributed to Motowo Mizuno.

42 records · Page 3Linked to original sources

PubMed2002

Improvements in the measurement of stool decay-accelerating factor in the detection of colorectal cancer.

We have previously developed an enzyme-linked immunosorbent assay (ELISA) to measure stool decay-accelerating factor (DAF) and found that stool DAF concentrations were significantly elevated in patients with colorectal cancer, suggesting that the measurement of stool DAF may be valuable for the detection of colorectal cancer. In order to refine the assay for the measurement of stool DAF, we investigated 1) effects of centrifugation of stool samples, 2) effects of detergents, and 3) adequate combination of various anti-DAF monoclonal antibodies for the ELISA system using only monoclonal antibodies. We found that high-speed centrifugation could be omitted and that only the removal of large undigested food residues by centrifugation of short duration in a low-speed benchtop microcentrifuge sufficed to adequately prepare the stool samples. Addition of 2 detergents, octyl beta-glucoside and sodium deoxycholate, known to solubilize glycosyl-phosphatidylinositol-anchored proteins such as DAF, did not influence stool DAF values. By using 2 mouse anti-DAF monoclonal antibodies (clone 4F11 and 1C6), we were able to achieve a stable ELISA for the measurement of stool DAF using a uniform source of antibodies. The results should allow us to consistently apply the DAF assay for routine use in the detection of colorectal cancer.

Aged↗

PubMed2002

Anti-asialoglycoprotein receptor autoantibodies, detected by a capture-immunoassay, are associated with autoimmune liver diseases.

In autoimmune chronic active hepatitis (AIH) and primary biliary cirrhosis (PBC), various autoantibodies including anti-asialoglycoprotein receptor (ASGPR) antibodies have been found in patients' sera. We have previously developed a mouse monoclonal antibody against rat and human ASGPR. In this study, we developed a capture enzyme-linked immunosorbent assay (ELISA) for detection of anti-ASGPR antibodies using this monoclonal antibody and investigated the occurrence of anti-ASGPR antibodies in the sera of patients with various liver diseases. Serum samples were obtained from 123 patients with various liver diseases, including 21 patients with AIH and 40 patients with PBC. In this capture ELISA, the target antigen in the crude rat liver membrane extracts was captured on the ELISA wells by the ASGPR-specific mouse monoclonal antibody. Thus, the cumbersome process of antigen purification was rendered unnecessary. Using this capture ELISA, we detected the anti-ASGPR antibody in 67% of the patients with AIH, in 100% of the patients with PBC, and in 57% of the patients with acute hepatitis type A. However, the anti-ASGPR antibody was rarely detected in patients with other liver diseases such as primary sclerosing cholangitis and obstructive jaundice. Our findings suggest that this capture ELISA would be useful for the detection of anti-ASGPR antibodies in autoimmune liver diseases.

Adolescent↗

PubMed2002

Development of syngeneic monoclonal anti-idiotype antibodies to mouse monoclonal anti-asialoglycoprotein receptor antibody.

Anti-idiotype antibodies (Ab2) play an important role in the homeostasis of immune responses and are related to the development and the disease activity of certain autoimmune diseases. The asialoglycoprotein receptor (ASGPR) is considered one of the target antigens in the pathogenesis of autoimmune chronic active hepatitis (AIH). We previously developed a mouse monoclonal antibody (clone 8D7) which recognizes rat and human ASGPR. In this study, to help investigate the anti-ASGPR antibody-anti-idiotype antibody network in patients with AIH, we developed a syngeneic mouse monoclonal Ab2 to the 8D7 anti-ASGPR antibody (Ab1). One clone, designated as 3C8, tested positive for specific reactivity to 8D7-Ab1 and did not bind to other irrelevant immunoglobulins. By competitive inhibition assays, the binding of 8D7-Ab1 to liver membrane extracts, i.e., the crude antigen preparation, was inhibited by 3C8-Ab2 in a dose-dependent manner, and the binding of 8D7-Ab1 to 3C8-Ab2 was inhibited by the liver membrane extracts. In the immunohistochemical analysis, 3C8-Ab2 blocked the specific staining of sinusoidal margins of rat hepatocytes by 8D7-Ab1. These results suggest that 3C8 anti-idiotype antibody recognizes the specific idiotypic determinants within the antigen-binding site of 8D7-Ab1.

Animals↗

PubMed2002

[Effect of antiulcer agents on the urea breath test--Comparison between rebamipide and ecabet sodium].

In this study, we assessed whether standard doses of antiulcer drugs rebamipide, and ecabet sodium influence the accuracy of the urea breath test (UBT). Without medication, values of UBT estimated with nondispersive isotope-selective infrared spectrometry did not significantly change during follow-up (average 4.4 months). Then, we randomized 21 H. pylori-positive patients without serious disease to receive either rebamipide or ecabet sodium for 28 days. UBT was performed at baseline, on day 14, on day 28, and 2 weeks after cessation of drugs. On day 14, the median value of UBT declined significantly (p = 0.0113) compared to baseline with ecabet sodium but not with rebamipide. This caused a false-negative result of UBT in one of 11 patients who received ecabet sodium. The decline of UBT resolved 2 weeks after drug cessation. In addition, we performed a crossover study in 11 H. pylori-positive volunteers with these drugs, and ecabet sodium but not rebamipide significantly reduced UBT values (p = 0.0058). These findings indicate that ecabet sodium adversely influences the accuracy of UBT and that the withdrawal of this drug before testing appears to be necessary to avoid false-negative results.

Abietanes↗

PubMedDate not supplied

Outcome of patients with inconsistent results from 13C-urea breath test and bacterial culture at the time of assessment of Helicobacter pylori eradication therapy in Japan.

BACKGROUND/AIMS: At the assessment of eradication therapy of Helicobacter pylori, the results of 13C-urea breath test and other methods such as bacterial culture are occasionally inconsistent. In this study, we examined the outcomes of inconsistent results. METHODOLOGY: Four hundred and four patients with peptic ulcer who were H. pylori-positive and who had completed eradication therapy were studied. Bacterial culture, rapid urease tests and 13C-urea breath test were performed between one and three months after the end of the therapy. The cut-off value for the 13C-urea breath test used originally in this study was 2.5 per mil. We investigated the outcome of inconsistent results by following up the patients every 6 to 12 months. RESULTS: At the initial assessment of eradication therapy, we observed inconsistent results with bacterial culture and 13C-urea breath test in 43 of 404 patients. Most of them (40 of 43) were culture-negative but urea breath test-positive, and the majority became negative for both tests. Based on the follow-up results, the optimum value for 13C-urea breath test at the assessment of eradication therapy was found to be 3.5 per mil. CONCLUSIONS: We found that outcomes of inconsistent results were variable, indicating the importance of the follow-up of patients after eradication therapy of H. pylori.

Breath Tests↗

PubMedDate not supplied

H. pylori decreases gastric mucin synthesis via inhibition of galactosyltransferase.

BACKGROUND/AIMS: Alterations of gastric mucin have been postulated as important pathogenic properties of Helicobacter pylori. In this study, we investigated gastric mucin synthesis in H. pylori-infected gastric mucosa by measuring UDP-galactosyltransferase activity, a key enzyme for the synthesis of mucin, and the amount of intracellular mucin in the gastric mucosa. METHODOLOGY: Gastric biopsy specimens were obtained from thirty-seven patients (20 H. pylori-positive and 17 H. pylori-negative). UDP-galactosyltransferase activity of the biopsy specimens was measured by an assay system we had developed, using a peanut agglutinin lectin. The amount of intracellular mucin in the gastric epithelial cells was analyzed by measuring the cells' periodic acid-Schiff-alcian blue staining-positive substances. RESULTS: UDP-galactosyltransferase activities in the antral mucosa, but not in the body mucosa, of H. pylori-positive patients were significantly lower than those of H. pylori-negative patients (p < 0.05). The amount of intracellular mucin in antral epithelial cells of H. pylori-positive patients was significantly lower than that of H. pylori-negative patients (p < 0.01). CONCLUSIONS: These findings suggest that H. pylori infection decreases gastric mucin synthesis via inhibition of UDP-galactosyltransferase. This effect may impair the gastric mucosal barrier and contribute to the mucosal injury induced by H. pylori infection.

Adult↗