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Biomedical subjects

T Koga

Publications and source records attributed to T Koga.

At least 739 records · Page 41Linked to original sources
PubMed1980

Giant cell carcinoma arising in a pulmonary bulla.

A 57-year-old male showed an abnormal mass shadow in a pulmonary bulla. Thoracotomy was performed and it was ascertained histologically that the tumour was a giant cell type carcinoma. Clinical features, histological findings and prognosis are reported.

Carcinoma↗
PubMed1979

Correlation between sectional area of the spleen by ultrasonic tomography and actual volume of the removed spleen.

The sectional area of the splenotomogram scanned parallel to the ribs provides useful information for differential diagnosis and determination of prognosis in liver diseases. To establish a relationship between sectional area and actual spleen volume, 10 spleens obtained at splenectomy or autopsy were studied. A good linear correlation (r = 0.956) was present between the sectional area (S) and the actual spleen volume (V). The spleen volume could be calculated as V = 7.5S - 77.5. Therefore the value of the sectional area obtained from one ultrasonic splenotomogram has practical application as a parameter reflecting the spleen volume in vivo.

Adult↗
PubMed1979

Cariogenic virulence of Streptococcus mutans AHT mutants with altered in vitro adherence abilities in hamsters.

Plaque-forming ability and cariogenic virulence of Streptococcus mutans AHT mutants having varying in vitro adherence abilities were studied in hamsters reared on a high sucrose diet over a period of 64 days. The parent wild-type strain produced heavy plaque and extensive carious lesions on molars. However, mutants M1, M2, and M13, which have lost the ability to form adhesive deposits on glass when grown in sucrose broth, and mutant M9, which adheres firmly to glass but in an extremely small amount, could not be recovered from the mouths of animals even after repeated inoculations at weekly intervals throughout the experimental period. Mutant M35, which produces a large amount of loosely adhering deposits in vitro, became established and persisted on molars, but its recovery was extremely low. None of the mutants, including M35, significantly produced plaque and caries in hamsters. Possible causes of this inability to form plaque and the avirulence of mutants are discussed.

Adhesiveness↗
PubMed1979

Inhibition of macrophage migration by muramyl peptides.

In the capillary tube migration system a synthetic muramyl dipeptide (MDP; N-acetylmuramyl-L-alanyl-D-isoglutamine), a part of bacterial cell wall peptidoglycans, inhibited the migration of peritoneal exudate macrophages from normal guinea pigs or rats. The migration inhibition was also caused by some MDP-containing peptidoglycan fragments from cell walls of Lactobacillus plantarum and Staphylococcus epidermidis. The migration inhibition could not be explained on the basis of macrophage migration inhibitory factor. A stereochemically highly specific structure of MDP required for its adjuvant activity was also required for the macrophage migration inhibition. These findings suggest that MDP and MDP-containing cell wall fragments may activate macrophages and that this activation may be important in the exertion of their adjuvant activity.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1979

Fractionation and properties of glucans produced by Streptococcus mutans.

Water-insoluble (ISG) and water-soluble (SG) fractions of glucans produced by cell-free glucosyltransferase of Streptococcus mutans AHT (serotype g) were isolated by centrifugation at 20,000 x g for 15 min. No further resolution of slightly sonicated ISG was observed with gel filtrations on any Bio-Gel beads, including A-50m. Bio-Gel P-100 filtration subdivided SG into two fractions with higher and lower molecular weights (designated SG-A and SG-B, respectively). SG-A was further resolved into two subfractions, SG-A-I and SG-A-II, by 10 to 40% and 50 to 80% ethanol precipitation, respectively. Relative amounts of ISG, SG-A-I, SG-A-II, and SG-B were 66.3:9.4:4.4:19.9. The molecular sizes of these fractions were >1.5 x 10(7), >==1.5 x 10(7), <==5 x 10(6) (>1 x 10(5)), and <==1 x 10(4) daltons, and their alpha-1,3 glucosidic linkage contents were approximately 35, 35, 16, and 4% for fractions ISG, SG-A-I, SG-A-II, and SG-B, respectively. Both ISG and SG-A-I were resistant to hydrolysis by dextranase and possessed the ability to aggregate with concanavalin A and to agglutinate S. mutans cells. SG-A-II had extremely low dextranase susceptibility and significant agglutinating activities, whereas SG-B showed high dextranase sensitivity and neither aggregating nor agglutinating activity. These results indicate that SG of S. mutans AHT consists of three types of glucans with distinctly different molecular sizes and chemical structures and strongly suggest that the ISG and SG-A-I fractions are different physical states of an inherently identical glucan. Preliminary observations suggest that the glucans produced by other S. mutans strains of several serotypes may be similarly classified.

Agglutination↗
PubMed1978

Cellular adherence, glucosyltransferase adsorption, and glucan synthesis of Streptococcus mutans AHT mutants.

Streptococcus mutans AHT mutants M1, M2, and M13 failed to adhere to a glass surface, whereas mutants M9 and M35 exhibited decreased and increased adherence, respectively, as compared with the parent strain, when grown in sucrose broth. Extracellular glucosyltransferase prepared from glucose-grown cultures of the adherent strains (wild type, M9, and M35) induced adherence of heat-killed cells of the homologous and heterologous streptococcal strains as well as of Escherichia coli K-12 and uncoated resin particles. The glucosyltransferase was adsorbed on all the streptococcal cells and glucan-coated resins, but not on E. coli cells and the uncoated resins. Glucosyltransferase from the nonadhering mutants (M1, M2, M13) neither was significantly adsorbed on nor induced adherence of any of the cells and resins. Cell-free enzymes from the glucose-grown adherent strains produced water-soluble and water-insoluble glucans, whereas those from the nonadhering mutants produced only water-soluble glucans. Small amounts of alkali-soluble, cell-associated glucan were recovered from the sucrose-grown nonadhering mutants. Thus, the relative proportions of glucosyltransferase isozymes elaborated by the S. mutans mutants, insofar as they affect the physico-chemical properties of the glucans produced, seem to determine the adherence abilities of the cells. The adsorption of glucosyltransferase on glucan molecules on the cell surface is not required for the adherence of S. mutans, but de novo glucan synthesis is important in the adherence process.

Adhesiveness↗
PubMed1978

Role of T lymphocytes in adjuvant arthritis. II. Different subpopulations of T lymphocytes functioning in the development of the disease.

The effects of treatments with cyclophosphamide (CY), hydrocortisone and anti-thymocyte sera (ATS) on the development of adjuvant arthritis (AA) were examined in WKA rats inoculated with wax D to induce AA. A single injection of 25 to 50 mg/kg of CY given 2 to 3 days before wax D inoculation caused severe arthritis with high incidence, whereas larger doses of CY were less efficient. Furthermore, the enhancing effect of CY pretreatment was abolished by passively transferred normal syngeneic thymocyreated with ATS and guinea pig C. On the basis of these results and the previous observations on the effect of adult thymectomy and low-dose irradiation, we concluded that this enhancing effect of CY pretreatment was caused by selective depletion of suppressor T lymphocytes. Pretreatment with 12.5 mg of hydrocortisone also caused severe arthritis. This enhancing effect of hydrocortisone could also be due to the elimination of those suppressor cells. In contrast, in vivo pretreatment with ATS showed striking inhibition on the development of AA, suggesting that ATS could eliminate T lymphocytes that were responsible for eliciting this disease. Thus it appears that at least two T cell subpopulations are involved in the development of AA, one is an ATS-sensitive T2 subpopulation that is effective for induction of AA and the other is a T1 subpopulation that regulates this disease process.

Animals↗