Search PubMed⌕ Search

Biomedical subjects

S Toyama

Publications and source records attributed to S Toyama.

At least 73 records · Page 4Linked to original sources
PubMed1985

Streptomyces beta-alanine:alpha-ketoglutarate aminotransferase, a novel omega-amino acid transaminase. Purification, crystallization, and enzymologic properties.

An enzyme which catalyzes the transamination of beta-alanine with alpha-ketoglutarate was purified to homogeneity from Streptomyces griseus IFO 3102 and crystallized. Molecular weight of the enzyme was found to be 185,000 +/- 10,000 by a gel-filtration method. The enzyme consists of four subunits identical in molecular weight (51,000 +/- 1,000). The transaminase is composed of 483 amino acids/subunit containing 7 and 8 residues of half-cystine and methionine, respectively. The enzyme exhibits absorption maxima at 278 and 415 nm. The pyridoxal 5'-phosphate content was determined to be 4 mol/mol of enzyme. The enzyme catalyzes transamination of omega-amino acids including taurine and hypotaurine. beta-Alanine and DL-beta-aminoisobutyrate served as a good amino donor; the Michaelis constants are 8.0 and 12.5 mM, respectively. alpha-Ketoglutarate is the only amino acceptor (Km = 4.0 mM); pyruvate and oxalacetate are inactive. Based on the substrate specificity, the terminology of beta-alanine:alpha-ketoglutarate transaminase is proposed for the enzyme. Carbonyl reagents, HgCl2,DL-gabaculine, and alpha-fluoro-beta-alanine strongly inhibited the enzyme.

4-Aminobutyrate Transaminase↗
PubMed1985

4-Aminobutyrate:2-oxoglutarate aminotransferase of Streptomyces griseus: purification and properties.

4-Aminobutyrate: 2-oxoglutarate aminotransferase of Streptomyces griseus was purified to homogeneity on disc electrophoresis. The relative molecular mass of the enzyme was found to be 100 000 +/- 10 000 by a gel filtration method. The enzyme consists of two subunits identical in molecular mass (Mr 50 000 +/- 1000). The transaminase is composed of 486 amino acids/subunit containing 10 and 12 residues of half-cystine and methionine respectively. The NH2-terminal amino acid sequence of the enzyme was determined to be Thr-Ala-Phe-Pro-Gln. The enzyme exhibits absorption maxima at 278 nm, 340 nm and 415 nm with a molar absorption coefficient of 104 000, 11 400 and 7280 M-1 cm-1 respectively. The pyridoxal 5'-phosphate content was calculated to be 2 mol/mol enzyme. The enzyme has a maximum activity in the pH range of 7.5-8.5 and at 50 degrees C. The enzyme is stable at pH 6.0-10.0 and at temperatures up to 50 degrees C. Pyridoxal 5'-phosphate protects the enzyme from thermal inactivation. The enzyme catalyzes the transamination of omega-amino acids with 2-oxoglutarate; 4-aminobutyrate is the best amino donor. The Michaelis constants are 3.3 mM for 4-aminobutyrate and 8.3 mM for 2-oxoglutarate. Low activity was observed with beta-alanine. In addition to omega-amino acids the enzyme catalyzes transamination with ornithine and lysine; in both cases the D isomer is preferred. Carbonyl reagents and sulfhydryl reagents inhibit the enzyme activity. Chelating agents, non-substrate L and D-2-amino acids, and metal ions except cupric ion showed no effect on the enzyme activity.

4-Aminobutyrate Transaminase↗
PubMed1985

Epicardial isopotential mapping from body surface isopotential mapping in myocardial infarction.

It is useful to construct the epicardial isopotential mapping (the Ep Map) from the body surface isopotential mapping (the Body Map) for clinical diagnosis of cardiac disease, even though there are many unsolved problems in using the inverse solution. Yamashita et al. carried out this solution by using the finite element technique. In the present study, the clinical value of that method has been investigated in cases of myocardial infarction. The Ep Maps at 20, 25 and 30 msec. from the beginning of the QRS complex were obtained from the Body Map at the same time by using that method; the infarcted areas on the Ep Map were determined by using Toyama's method which was reported in a previous study. The infarcted area at 30 msec. on the Ep Map was located at the anterior wall along the ventricular septum in anterior infarction and at the posterior wall of the left ventricle in inferoposterior infarction. Patients were independently examined with the scintigram with thallium-201 and the infarcted area was coincident to the location of the abnormal findings of the scintigram. Moreover, the size of the infarcted area on the Ep Map and the size of the abnormal findings of the scintigram were parallel in most cases except one.

Electrocardiography↗
PubMed1984

A variant form of beta-actin in a mutant of KB cells resistant to cytochalasin B.

Lines of KB cells resistant to cytochalasin B have been isolated and characterized. The mutant Cyt 1 exhibits increased cross-resistance to cytochalasin E. Cyt 1 cells bind less cytochalasin B than parental KB cells. Two-dimensional gel analysis shows that Cyt 1 cells carry an alteration in beta-actin. This is further confirmed by one-dimensional peptide analysis. The altered beta-actin (beta'-actin) is synthesized when poly(A)+ RNA from Cyt 1 cells is translated in a reticulocyte-cell-free translation system. These results suggest that the primary site of action of cytochalasin B on cellular motility processes is beta-actin.

Actins↗
PubMed1984

A comparative study of body surface isopotential mapping and the electrocardiogram in diagnosing of myocardial infarction.

It is important to determine the location of the infarcted area by body surface isopotential mapping (MAP), but at present there is no definite method to accomplish this. The present authors reported that they were able to estimate the infarcted area by MAP, and so it became necessary to confirm the reliability of their method. Initially, in a retrospective study using 50 cases, a comparison was made between the location of the infarcted area estimated by MAP and that estimated by 12-lead ECG to determine the size of the infarcted area of a region in which positive findings were obtained to determine the location of infarction. Criterion A (the infarcted area occupies more than half of a region in which positive findings are obtained by MAP) in a previous study was too severe for MAP, and Criterion B (the infarcted area occupies more than one third of a region in which positive findings are obtained) was adequate as a positive finding by MAP after comparison with the 12-lead ECG. This was confirmed in 40 cases in a prospective study. Secondly, in order to assess the superiority of MAP to the 12-lead ECG, the sensitivity, specificity and others of MAP and those of the 12-lead ECG to a scintigram using thallium-201 (SCG) were calculated. The sensitivity and negative predictive value of MAP to SCG were superior to that of ECG to SCG in the lateral, inferior and posterior walls, and it was suggested that MAP was more sensitive than 12-lead ECG in detecting the location of myocardial infarction.

Electrocardiography↗
PubMed1984

Relation between the location of the infarcted area in body surface isopotential mapping and the location of myocardial infarction in vectorcardiography.

In order to examine whether our method of determining the location of the infarcted area in body surface isopotential mapping (MAP) is adequate for clinical use, a comparison was made between the location of the infarcted area using MAP and the location of myocardial infarction using vectorcardiography (VCG). The percentage of agreement between MAP and VCG in the retrospective study was 91.7% in the anterior wall, 76.7% in the lateral wall, 93.3% in the inferior wall and 73.3% in the posterior wall. The reason for the disagreement between these two methods was investigated, and criteria for determining the infarcted area using MAP and vectorcardiographic criteria for myocardial infarction were partly corrected in anterior, lateral and (high) posterior infarction to increase the clinical accuracy of both methods. Consequently, the percentage of agreement in the four walls ranged from 83.7% to 87.9%, and the diagnostic value of MAP for the infarcted area was not inferior but was more sensitive than that of VCG except in anterior infarction. In the prospective study, the same result was obtained. Secondly, in order to establish the superiority of MAP or VCG, the sensitivity and specificity of MAP and VCG to SCG (thallium-201) were calculated. Except in the anterior wall, the sensitivity of MAP to SCG was higher than that of VCG to SCG, especially in the lateral and posterior walls. Accordingly, it is suggested that MAP is the method of choice in determining the infarcted area in clinical cases.

Electrocardiography↗
PubMed1984

In vivo radiolocalization of antiosteogenic sarcoma monoclonal antibodies in osteogenic sarcoma xenografts.

Monoclonal antibodies Ost6 and Ost7 (mouse Immunoglobulin G1) to human osteogenic sarcoma were isolated from ascitic fluid and labeled with radioiodine. After injection into athymic nu/nu mice with s.c. xenografts of human osteogenic sarcoma, the uptake of radioactivity in tumors, visceral organs, and blood was determined. Five days after injection, Ost6 and Ost7 showed preferential accumulation in tumors (tumor:blood ratio, 4.3). Furthermore, with testicular and bladder tumors, both unreactive with Ost7, there was no localization of radiolabeled Ost7 in xenograft growths. When Ost7 was labeled with 131I, its accumulation into human osteogenic sarcoma could be clearly visualized by whole-body gamma-scintigraphy without computer-assisted data processing.

Animals↗
PubMed1984

[Experimental and clinical studies on esophago-gastric hemodynamics before and after devascularization for esophageal varices].

Esophago-gastric hemodynamics subsequent to devascularization was studied in a view of changes in mucosal blood flow and tissue oxygen tension (PtO2). Thirty-four mongrel dogs (26 normal dogs and 8 portal hypertensive dogs) were used in experimental studies, and mucosal blood flow was determined by means of hydrogen gas clearance. Remarkable reduction of a 73% in gastric cardia was recognized on normal dogs just after extended devascularization, and those dogs died of severe gastric necrosis within 4 days after surgery. Reduction of a 28.5% in the cardia was found by the devascularization on portal hypertensive dogs produced by a whole liver compression. These portal hypertensive dogs survived for 2 weeks after surgery, and then mucosal blood flows were returned to the previous levels. Liver cirrhosis (10 cases) with esophageal varices were used for clinical studies. Gastric hemodynamics was measured by PtO2 before and after devascularization. Reduction of a 25.7% in the cardia was recognized on cirrhotic patients. These results suggest that influences of extended devascularization on esophago-gastric hemodynamics would be a small in cirrhotic patients with esophageal varices.

Animals↗
PubMed1983

Deficient cytidine monophospho-N-acetylneuraminic acid: glycoprotein sialyltransferase activity in a clone of KB cells with altered cell fusion ability.

Lines of KB cells resistant to Sendai virus-induced cytolysis have been isolated and characterized (Toyama, S., Toyama, Su., and Uetake, H. (1977) Virology 76, 503-515). This study is concerned with the nature of this mutation. Plasma membrane fractions from Sil cells were found to have decreased amount of sialic acid and the same amount of galactose as compared to the membranes from parental KB cells. Sil cells exhibited an increase in sensitivity to toxic effects of ricin and a decrease in sensitivity to wheat germ agglutinin. Binding of wheat germ agglutinin to Sil cells was markedly decreased. Several membrane glycoproteins of Sil cells migrated slightly faster than the corresponding bands of wild type membrane when examined by gel electrophoresis in sodium dodecyl sulfate. Sil cells had decreased sialyltransferase activity that catalyzed the transfer of sialic acid residues from CMP-N-acetylneuraminic acid to glycoprotein acceptors containing Gal beta 1 leads to 3GalNAc alpha 1 leads to O-Ser(Thr) chain. The decreased enzyme activity could not be accounted for by the presence of inhibitors, altered pH optimum, or increased sialidase or CMP-sialic acid hydrolase activities. These results indicate that a molecular basis for the Sil cell phenotype might be the deficiency of sialyltransferase.

Animals↗
PubMed1983

[Detection of human osteosarcoma-associated antigens by monoclonal antibodies].

Hybrid cell lines have been derived from a fusion between mouse myeloma cell line, NS1/Ag 4-1, and spleen cells from BALB/c mice immunized with freshly resected osteosarcoma cells from an untreated patient. Of the 276 hybrids obtained, five secreted antibodies which bound to osteosarcoma tissues but not to autologous skin fibroblasts. Antibodies secreted by individual hybrids were tested for their reaction with a panel of human normal and tumor tissues in an immunofluorescence assay, and they displayed different specificities. Two of these antibodies, OST2 and OST4, bound to osteosarcoma tissues and to some other tumors and normal tissues. The antibodies from three of these five hybrids, OST6, OST7, and OST15, reacted with all of seven osteosarcoma tissues and one chondrosarcoma tissue but not with other malignant or benign tumors. Tests of various normal tissues were negative, except for weak binding to a subpopulation of chondrocytes in calcified areas of cartilage near the subchondral bone. Interestingly, none of the antibodies showed reactivity with three osteosarcoma cell lines, Te 85, Te 418, and MG 63. The experiments established the usefulness of the hybridoma technique in preparing monospecific antibodies against human osteosarcoma associated antigens. In particular, this study demonstrates that the use of freshly resected tumor tissues in preparing monoclonal antibodies would provide a necessary tool for the study of tumor associated antigens.

Adolescent↗
PubMed1982

The body surface isopotential mapping of the QRS wave in myocardial infarction. a comparative study of the scintigram with thallium-201.

When body surface isopotential mapping (MAP) is used in clinical cases of myocardial infarction, it is necessary to determine the location of the infarcted area. The present authors presumed that the positive area of MAP in normal subjects, which was altered to a negative area of MAP in myocardial infarction, was the infarcted area. In order to confirm the presumed location of the infarcted area, the location of the infarcted area on MAP and the location of infarction presumed by the scintigram with thallium-201 (SCG) were compared. MAP was divided into ten regions and a comparison between the presence or absence of an infarcted area in each segment on the MAP and of abnormal findings in each segment of the SCG was made. Consequently, the highest percentage of agreement in each region of the segment in SCG was picked up, and each region on MAP which corresponded to the segment in SCG was determined. Thereafter, each segment of MAP was matched with a wall of the ventricle: region 1--the septum; region 2--the apex; region 3--the anterior wall; region 4--the posterior portion of the apex; the upper portion of region 5--the lateral wall; region 6, 8 and 10--the inferior wall; and region 7--the posterior wall. In this way, the classification of myocardial infarction was carried out in 51 cases.

Electrocardiography↗