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Biomedical subjects

S Shiga

Publications and source records attributed to S Shiga.

54 records · Page 3Linked to original sources
PubMed1984

Infectivity titration of hemorrhagic fever with renal syndrome virus: use of immune adherence hemagglutination for detection of virus growth.

Serial dilutions of hemorrhagic fever with renal syndrome viruses were inoculated into Vero-E6 cells in microplates. After 2 weeks of incubation, infected cells were disrupted by freezing and thawing, and virus antigens were detected by immune adherence hemagglutination. The infectivity titers of the virus as determined by this method were in close agreement with those obtained by the immunofluorescent antigen endpoint method. Then, a neutralization method was established. Japanese hemorrhagic fever with renal syndrome isolates, strains SR-11 and TR-352, were found to be distinct from Hantaan virus, strain 76-118, by the neutralization test.

Animals↗
PubMed1983

Genetic determinant of pyocin R2 in Pseudomonas aeruginosa PAO. I. Localization of the pyocin R2 gene cluster between the trpCD and trpE genes.

Thirty-seven mutants defective in pyocin R2 production in the P. aeruginosa PAO strain were subjected to fine mapping of pyocin R2 genes by transduction with phage F116L. Sixteen complementation groups (designated prtA through prtP) involved in pyocin R2 production were tentatively identified by complementation tests using phage F116L. Their linkages to trpC and trpE markers and fine mapping by three point crosses demonstrated that most of the mutations (prtA through prtN) were located in between trpC and trpE, and that the prtP mutation was localized outside this major prt cluster but in the proximity of the rifA and strA region.

Bacteriocins↗
PubMed1983

Genetic determinant of pyocin R2 in Pseudomonas aeruginosa PAO. II. Physical characterization of pyocin R2 genes using R-prime plasmids constructed from R68.45.

The chromosome segment which contains the genes responsible for production of pyocin R2 in P. aeruginosa PAO was defined physically using R-prime plasmids constructed in vivo from R68.45. The previous conclusion from genetic mapping that the cluster of pyocin R2 genes is located in between trpC and trpE genes was confirmed by deletion mapping of various R prime plasmids bearing the trpC gene. The pyocin R2 gene cluster was further localized on two contiguous HindIII fragments of 16 kb and 8.0 kb. PML14 strain, in which R-type pyocin genes were completely deleted, had only one 11 kb HindIII fragment instead. Heteroduplexes between this 11 kb fragment with the two HindIII fragments of PAO revealed that the cluster of pyocin R2 genes was an insertion 13 kb long.

Bacteriocins↗
PubMed1983

Isolation of virus causing hemorrhagic fever with renal syndrome (HFRS) through a cell culture system.

Twenty-three rat lung specimens collected in outbreaks of hemorrhagic fever with renal syndrome (HFRS) in three medical institutions were inoculated onto the VERO-E6 cell monolayers. After several blind passages, an agent growing serially in the cell cultures and reacting specifically with known HFRS-positive sera was isolated from two of these specimens. The two isolates were antigenically identical each other. The agent, named strain SR-11, was identified as the causative virus of HFRS by its antigenic identity with E6 cell-adapted HFRS virus, Hantaan 76-118 strain, and the specific reactions with sera from various HFRS cases.

Adolescent↗
PubMed1980

Effect of iron concentration in the growth medium on the sensitivity of Pseudomonas aeruginosa to pyocin S2.

The iron concentration in the growth medium was found to affect the susceptibility of Pseudomonas aeruginosa PML1550 to pyocin S2, a bacteriocin. The efficiency of killing by pyocin S2 was very low when the indicator cells were grown in an iron-rich medium. The capacity of these cells to adsorb pyocin S2 was reduced. Cultivation under limitation of iron (1 microM or less) was necessary to produce a fully sensitive cell population. The growth under iron limitation was accompanied by the appearance of four protein components in the outer membrane of the cells. Nine mutants resistant to pyocin S2 were isolated and their outer membranes were analyzed. They all lacked one component (Fe-b protein) as well as the adsorption capacity for pyocin S2. These findings suggest a possible role of this protein as the receptor for pyocin S2.

Bacteriocins↗
PubMed1979

An esterase on the outer membrane of Pseudomonas aeruginosa for the hydrolysis of long chain acyl esters.

A new esterase activity which hydrolyzes palmitoyl-CoA was found in the membrane fraction of Pseudomonas aeruginosa. All the 11 strains of P. aeruginosa tested possessed this esterase activity. The esterase was constitutive and was fully active on the intact cell bodies toward substrates in the medium. It was located on the outer membrane of the cell envelope, and was not released into the culture medium. This activity was designated as OM (outer membrane) esterase. OM esterase was solubilized from the cell envelope with EDTA-Triton X-100 and purified 690-fold. It was a minor component of the outer membrane. Its molecular weight was approximately 55,000. The activity was rather stable to heat, a wide range of pH, and treatment with detergents and organic solvents. No cofactors were required. The pH optimum of the reaction was 8.5. Among various acyl-CoAs, only long chain (C12--C18) thioesters were hydrolyzed. OM esterase also hydrolyzed some kinds of oxy-esters such as p-nitrophenyl acyl esters, monoacyl esters of sucrose and Tween 80 (polyoxyethylene sorbitan monooleate). On the other hand, triglycerides, phospholipids, or hydrophobic monoesters were not hydrolyzed at all. Thus, this enzyme seems to have specificity for long chain acyl esters with hydrophilic groups, whether thio- or oxy-ester. Mutants deficient in this esterase activity were isolated. These mutants were unable to grow on Tween 80 as a sole carbon source. This suggests a possible role of OM esterase in the utilization of acyl esters as carbon sources.

Acyl Coenzyme A↗
PubMed1979

Bactericidal activity of the tail of Pseudomonas aeruginosa bacteriophage PS17.

The tail of bacteriophage PS17 of Pseudomonas aeruginosa was shown to be bactericidal, and its properties were compared with those of pyocin R1. Temperature-sensitive mutants were isolated from PS17, and the products at nonpermissive temperature were morphologically characterized. Bactericidal substances were found in the lysates of such mutants that were defective in the head formation but not in the tail formation. Phage tails were purified from the lysate of one such mutant, and its chemical and biological properties were studied. Isolated tails killed sensitive cells by a single-hit process and repressed the uptake of leucine in sensitive cells. These results were consistent with the previous findings on the serological and morphological relationship between PS17 and pyocin R1. However, certain differences were also shown between them in shape and protein composition.

Antigens, Viral↗
PubMedDate not supplied

Lack of plasma leptin response to feeding in newborn infants.

OBJECTIVE: Previous reports of the postprandial regulation of leptin are controversial, and there have been few studies on the effects of breast-feeding on postprandial regulation in newborn infants. We examined the response of plasma leptin to breast- and formula-feeding in newborn infants. METHODS: We measured the plasma leptin levels using an enzyme-linked immunosorbent assay kit before and after feeding in 12 breast-fed and 11 formula-fed mature infants. RESULTS: There was no significant difference in plasma leptin levels in breast-fed infants before and after feeding or in artificially fed infants before and after feeding. CONCLUSION: Our results suggest that feeding does not play a role in the acute response of circulating leptin levels in either breast- or formula-fed infants.

Breast Feeding↗
PubMedDate not supplied

In vitro analysis of the change in resistance of Chlamydia trachomatis under exposure to sub-MIC levofloxacin for a therapeutic term.

BACKGROUND: While fluoroquinolone-resistant Chlamydia trachomatis strains have not been clinically isolated, they were isolated in an in vitro study recently. METHODS: To determine whether C. trachomatis strains develop resistance under sub-MIC antibacterial exposure in a clinical therapeutic term, C. trachomatis strains were exposed to sub-MIC levofloxacin (LVFX) for about 2 weeks. The MIC of LVFX was measured and DNA fingerprinting was performed every 72 h by PCR using random primers. RESULTS: There was almost no change in the MIC under exposure to 0.125 microg/ml LVFX. However, some mutational changes in DNA fingerprints developed. CONCLUSIONS: In clinical therapeutic terms, resistant strains of C. trachomatis will probably not develop, even if sub-MIC LVFX is employed.

Anti-Infective Agents↗