Yonsei University

About: Yonsei University is a education organization based out in Seoul, South Korea. It is known for research contribution in the topics: Population & Cancer. The organization has 50162 authors who have published 106172 publications receiving 2279044 citations. The organization is also known as: Yonsei.

Identification of Toxin A-Negative, Toxin B-Positive Clostridium difficile by PCR

Abstract: Toxigenic strains of Clostridium difficile have been reported to produce both toxins A and B nearly always, and nontoxigenic strains have been reported to produce neither of these toxins. Recent studies indicate that it is not always true. We established a PCR assay to differentiate toxin A-negative, toxin B-positive (toxin A-, toxin B+) strains from both toxin-positive (toxin A+, toxin B+) strains and both toxin-negative (toxin A-, toxin B-) strains as an alternative to cell culture assay and enzyme-linked immunosorbent assay (ELISA). By using the PCR primer set NK11 and NK9 derived from the repeating sequences of the toxin A gene, a shorter segment (ca. 700 bp) was amplified from toxin A-, toxin B+ strains compared to the size of the segment amplified from toxin A+, toxin B+ strains (ca. 1,200 bp), and no product was amplified from toxin A-, toxin B-strains. We examined a total of 421 C. difficile isolates by PCR. Of these, 48 strains showed a shorter segment by the PCR, were negative by ELISAs for the detection of toxin A, and were positive by cell culture assay. Although the cytotoxin produced by the toxin A-, toxin B+ strains was neutralized by anti-toxin B serum, the appearance of the cytotoxic effects on Vero cell monolayers was distinguishable from that of toxin A+, toxin B+ strains. By immunoblotting, the 44 toxin A-, toxin B+ strains were typed to serogroup F and the remaining four strains were serogroup X. Pulsed-field gel electrophoresis separated the 48 strains into 19 types. The PCR assay for the detection of the repeating sequences combined with PCR amplification of the nonrepeating sequences of either the toxin A or the toxin B gene is indicated to be useful for differentiating toxin A-, toxin B+ strains from toxin A+, toxin B+ and toxin A-, toxin B- strains and will contribute to elucidation of the precise role of toxin A-, toxin B+ strains in intestinal diseases.

Observation of the DsJ(2317) and DsJ(2457) in B Decays

Abstract: We report the first observation of the B-->(D) over barD(sJ)(2317) and B-->(D) over barD(sJ)(2457) decays based on 123.8x10(6) B (B) over bar events collected with the Belle detector at KEKB. We observe the D-sJ(2317) decay to D(s)pi(0) and the D-sJ(2457) decay to the D(s)(*)pi(0) and D(s)gamma final states. We also set 90% C.L. upper limits for the decays D-sJ(2317)-->D-s*gamma, D-sJ(2457)-->D-s*gamma, D-sJ(2457)-->D(s)pi(0), and D-sJ(2457)-->D(s)pi(+)pi(-).

Cryptococcus neoformans and Cryptococcus gattii, the Etiologic Agents of Cryptococcosis

Abstract: Cryptococcus neoformans and Cryptococcus gattii are the two etiologic agents of cryptococcosis. They belong to the phylum Basidiomycota and can be readily distinguished from other pathogenic yeasts such as Candida by the presence of a polysaccharide capsule, formation of melanin, and urease activity, which all function as virulence determinants. Infection proceeds via inhalation and subsequent dissemination to the central nervous system to cause meningoencephalitis. The most common risk for cryptococcosis caused by C. neoformans is AIDS, whereas infections caused by C. gattii are more often reported in immunocompetent patients with undefined risk than in the immunocompromised. There have been many chapters, reviews, and books written on C. neoformans. The topics we focus on in this article include species description, pathogenesis, life cycle, capsule, and stress response, which serve to highlight the specializations in virulence that have occurred in this unique encapsulated melanin-forming yeast that causes global deaths estimated at more than 600,000 annually.

Effect of obesity on total and free insulin-like growth factor (IGF)-1, and their relationship to IGF-binding protein (BP)-1, IGFBP-2, IGFBP-3, insulin, and growth hormone

Abstract: OBJECTIVES: We investigated the effect of obesity on the serum levels of total and free IGF-1 and their relationship to the circulating levels of insulin and IGF binding proteins (IGFBPs) in age and sex-matched groups. SUBJECTS: The study included 43 obese subjects (ideal body weight; IBW>120%) and 45 controls (IBW<100%). All of the subjects were male. MEASUREMENT: Total IGF-1, free IGF-1, IGFBP-1, IGFBP-2, IGFBP-3, and insulin were measured in obese subjects and normal control subjects. RESULTS: No significant differences in the circulating levels of total and IGFBP-3 were observed between the obese and control groups. In contrast to total IGF-1, free IGF-1 in obese subjects was significantly increased compared to normal controls (P<0.05). Serum total and free IGF-1 were inversely correlated with age (r=−0.42, P=0.001, and −0.44, P=0.001). Fasting serum insulin concentrations were elevated in all the obese subjects (P<0.05) and positively correlated with IBW (r=0.57, P=0.001). The levels of serum GH and IGFBP-1 were suppressed in all the obese subjects (P<0.05). IGFBP-1 was inversely correlated with IBW (r=−0.51, P=0.001) and serum insulin concentrations (r=minus;0.48, P=0.001). The IGFBP-2 concentrations were also suppressed in obese subjects and inversely related to free IGF-1 (r=−0.48, P=0.001). Using multiple linear regression analysis, total IGF-1 and insulin concentrations were positively correlated (r=0.58, P=0.001) and free IGF-1 and IGFBP-1 concentrations were negatively correlated (r=−0.57, P=0.001). CONCLUSION: We confirmed that total IGF-1 and IGFBP-3 concentrations were not significantly different between the obese and control groups, despite GH hyposecretion in obesity. We also found that free IGF-1 concentrations were higher in obese subjects than in normal controls. It seems likely that overnutrition and chronic hyperinsulinaemia in obesity may alter this regulated growth response by insulin stimulation of IGF-1 production and suppression of hepatic IGFBP-1 and IGFBP-2 production, which may inhibit IGF-1 bioactivity.