Biomedical subjects
M Yano
Publications and source records attributed to M Yano.
[On the drug resistance of microorganisms collected by paper-point method].
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[Uniqueness of nursing activities in a university affiliated hospital].
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Separation of a new substrate, kininogen-I, for plasma kallikrein in bovine plasma.
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An improved method for the purification of kininogen-II from bovine plasma.
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Partial purification of bovine plasma kallikrein activated by contact with glass.
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[Electroencephalographic studies on uremia. (1)].
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[Case of Addison's disease with repeated acute adrenal crisis].
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[The influence of obstetrical anesthesia upon the physical and mental developement of newborn infants].
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Chemistry of C-16-oxygenated 5-alpha,14-beta-androstanes.
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A study on the pearly layer formation of Clostridium botulinum.
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On adonitol fermenting ability of coliform bacilli.
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A basic study on culture of Veillonella in oral cavity.
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[Studies on a specific antigen in the serum of stomach cancer patients. 1. Serologic diagnosis of stomach cancer].
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Therapeutic ethanol injection of hepatocellular carcinomas undetectable by angiography and Lipiodol computed tomography.
Seven smaller than 2 cm in diameter hepatocellular carcinomas (HCC) undetectable by hepatic arteriography and computed tomography (CT) after intraarterial injection of iodized oil (Lipiodol CT) were diagnosed by ultrasonography-guided fine-needle biopsy in 6 patients. All lesions were treated by percutaneous ethanol injection (PEI) in 1-3 weekly intervals. No recurrences have been demonstrated after 7-15 months. The treatment of HCCs undetectable by angiography and Lipiodol CT presents a problem as transcatheter arterial embolization is considered ineffective due to poor vascularity. PEI appears to be an excellent treatment for these small HCCs.
Alterations of plasma immunoreactive glucagon-like peptide-1 behavior in non-insulin-dependent diabetics.
The basal level of plasma immunoreactive glucagon-like peptide-1 (IR GLP-1) was significantly elevated in non-insulin-dependent diabetics (NIDD), and this elevation of IR GLP-1 was mainly due to an increase in the large component of IR GLP-1, corresponding to the pancreatic form. During the oral glucose-tolerance test (OGTT), the total plasma IR GLP-1 decreased in normal subjects but increased significantly in diabetic patients. Chromatographic analysis showed that IR GLP-1 consisted of several different molecular forms. OGTT caused a decrease in the pancreatic form but increased the intestinal form in normal subject, resulting into a net decrease in total plasma IR GLP-1. Whereas in NIDD the increase in the intestinal form was more prominent and the suppression of the pancreatic form was practically abolished to result in a net increase of total plasma IR GLP-1. This observation is consistent with the fact that in normal subjects the total change in IR GLP-1 was significantly correlated with both the total change of gut glucagon as well as that of pancreatic glucagon, but in diabetics the total change of GLP-1 only correlated to that of gut glucagon. The impaired suppression of pancreatic GLP-1 and enhanced release of intestinal GLP-1 could have some physiological importance in NIDD.
Non-radioactive DNA diagnosis for the fragile X syndrome in mentally retarded Japanese males.
A rapid screening test was developed to detect CGG repeat expansion of the FMR-1 gene causing the fragile X syndrome by a non-radioisotope PCR technique. A biotin-labeled primer was initially used and the biotin-labeled PCR product was detected by means of chemiluminescence. The normal PCR product of around 300 bp was not created in the abnormal FMR-1 gene sample with this method. Four positive samples were found among those from 226 mentally retarded males, but the CGG repeat expansion was shown on Southern blot analysis in only one sample. To eliminate false-positive samples, a hybridization method involving a biotin-labeled (CGG)s oligonucleotide was developed for the PCR product and the CGG repeat expansion could be detected. Finally, 256 mentally retarded males in Japan were examined and only 2 abnormal samples were detected. The prevalence of this abnormality was less than 1%, which is relatively lower than those reported previously.
Helicobacter pylori may cause "reflux" gastritis after gastrectomy.
Patients with "reflux" gastritis after gastrectomy suffer from a variety of symptoms, and this type of gastritis may sometimes compromise the quality of life of these patients. Since Helicobacter pylori is considered to be one of the most important pathogenetic factors in gastritis, the association between H. pylori and reflux gastritis was investigated in this study. A total of 145 patients with gastrectomy were entered into the study. Five biopsy specimens from the gastric remnant were taken at upper gastrointestinal endoscopy. One specimen was examined pathohistologically, and the remaining four were examined for H. pylori infection. Fifty-two patients (36%) demonstrated H. pylori infection. The prevalence of H. pylori was significantly higher in patients who had a partial gastrectomy, and it was significantly lower in patients who had undergone gastrectomy more than 4 years previously. The histologic gastritis score in patients with H. pylori infection was significantly higher. Furthermore, H. pylori was eradicated in patients with some symptoms of gastritis and no bile reflux to the residual stomach at endoscopy; in these patients the symptoms were relieved and the histologic gastritis score decreased significantly. In conclusion, possible involvement of H. pylori is suspected in the pathogenesis of "nonreflux" gastritis after gastrectomy.