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Biomedical subjects

E Kondo

Publications and source records attributed to E Kondo.

At least 271 records · Page 15Linked to original sources
PubMed1966

Drug resistance of enteric bacteria. VI. Introduction of bacteriophage P1CM into Salmonella typhi and formation of PldCM and F-CM elements.

Kondo, Eiko (Gunma University, Maebashi, Japan), and Susumu Mitsuhashi. Drug resistance of enteric bacteria. VI. Introduction of bacteriophage P1CM into Salmonella typhi and formation of P1dCM and F-CM elements. J. Bacteriol. 91:1787-1794. 1966.-Bacteriophage P1CM was introduced into Salmonella typhi by means of both phage infection and conjugation with Escherichia coli F(+) lysogenic for the phage. Upon incubation with a P1CM phage lysate, S. typhi and S. abony yield CM(r) cells which are lysogenic for P1CM, but S. typhimurium LT2 does not. The P1CM phage is adsorbed slightly to S. typhi, but no infectious centers are formed when the phage is plated on this strain. Tests on P1CM-adsorbing capacity of the S. typhi P1CM(+) strain and on plaque formation and transduction ability of the recovered phage from this strain indicated that the cell and the phage population did not have any special advantage over the original cell and phage population. Conjugation of S. typhi with E. coli F(+) carrying P1CM(+) gave three types of S. typhi CM(r) clones: those which carry the whole P1CM phage, those with the P1dCM element, and those with nontransferable CM(r). The second type has the F factor and is sensitive to f phages in spite of its typical behavior, serologically and biochemically, as S. typhi. It can donate the P1dCM and F(+) characters to E. coli F(-) or F(-)/P1 strains. As a consequence of conjugation with the E. coli F(+) strain, the CM(r) character of the third type of S. typhi, the nontransferable CM(r) element, acquired conjugational transferability, owing to the formation of the element, F-CM. This element can be transferred to an E. coli F(-) strain at a very high frequency (ca. 10(0)). Both the F and CM(r) determinants are jointly transduced with P1 phage and are jointly eliminated by acridine dye treatment.

Drug Resistance, Microbial↗
PubMed1965

Mycoside G, a Specific Glycolipid in Mycobacterium marinum (Balnei).

Navalkar, R. G. (University of Wisconsin, Madison), E. Wiegeshaus, E. Kondo, H. K. Kim, and D. W. Smith. Mycoside G, a specific glycolipid in Mycobacterium marinum (Balnei). J. Bacteriol. 90:262-265. 1965.-A new specific glycolipid in extracts prepared from strains designated Mycobacterium marinum and M. balnei has been demonstrated by use of the techniques of column chromatography and infrared spectroscopy. Since there is now agreement among many workers that M. marinum and M. balnei are identical, the demonstration of the same specific glycolipid in both species is not surprising. This substance, which we have designated mycoside G, is chemically similar to mycosides A and B, and apparently differs only in the sugar moiety. In addition, the lipids extracted from these cultures contain phthiocerol dimycocerosate, a wax component found also in M. tuberculosis and M. bovis.

Journal Article↗
PubMedDate not supplied

Binding of human leukocytes to fibronectin is augmented by an anti-CD44 mAb (TL-1) and blocked by another anti-CD44 mAb (Hermes-3) but not by anti-VLA-4/VLA-5 mAbs.

Fibronectin (FN) forms meshworks in extracellular spaces, and it plays an important role in cellular trafficking. Lymphoid cells are activated by binding to FN of the VLA-4 and VLA-5 receptors. CD44 also acts as a receptor of FN, but the mechanism and physiologic regulation of their binding are poorly understood. We have developed an anti-CD44 monoclonal antibody (mAb) (TL-1) in which lymphoid cells are activated and form homotypic cell aggregation. In this study, we found that the adhesion of CEM, HSB2, and LAD lymphoid cells to FN was augmented by TL-1 treatment and was apparently blocked by another anti-CD44 mAb (Hermes-3), but TL-1 Fab' fragments treatment did not induce FN-binding. A similar phenomenon is reported in the binding of the CD44 molecule to HA. This augmentation was not inhibited by the CS1 and RGD peptides of FN or by anti-VLA-4 and -VLA-5 mAbs; it was energy-dependent and associated with cytoplasmic actin filaments. Tl-1 treatment did not alter the cell surface expression of CD44 molecules. These findings above suggested that activated and/or altered cell surface distribution of CD44 molecules via a conformational change augmented the avidity of its binding to FN, which may be similar to lymphocyte-hyaluronate and lymphocyte-endothelial cell binding. As the Hermes-3 binding site is also involved in the interaction between lymphocytes and endothelial cells, activation of lymphocytes via CD44 molecules may facilitate the binding of lymphocytes to endothelial cells, extravasation, and migration to inflammatory sites rich in FN.

Adjuvants, Immunologic↗
PubMedDate not supplied

Early ultrastructural changes in the central nervous system in Fukuyama congenital muscular dystrophy.

Electron microscopy of the central nervous system surface structure is described in two fetuses with Fukuyama congenital muscular dystrophy (FCMD). In addition to relatively large surface defects, many minute defects less than several micrometers in size associated with protrusion of glial cytoplasm were observed in the cerebrum. These findings were considered to represent early changes prior to cortical dysplasia. The basement membrane adjacent to the defects showed amorphous, wavy, or whorled configurations, and gradually disappeared. The glial cytoplasmic membrane seemed to be relatively well preserved in some areas where the basement membrane disappeared. On the other hand, both the basement membrane and cytoplasmic membrane became indistinct irregularly in areas without defects, including the spinal cord; similar lesions were found in the skeletal muscle. These observations confirm previous observations concerning defects of the pial-glial barrier of the brain surface, and may suggest the involvement of abnormal basement membrane or related structures, or both, in the genesis of the brain lesions of FCMD.

Adult↗