|1.||Bayer, Arnold S: 3 articles (05/2015 - 09/2002)|
|2.||Kreiswirth, Barry N: 2 articles (05/2015 - 12/2011)|
|3.||Seidl, Kati: 2 articles (05/2015 - 12/2011)|
|4.||Xiong, Yan Q: 2 articles (05/2015 - 12/2011)|
|5.||Yeaman, Michael R: 2 articles (05/2015 - 09/2002)|
|6.||Chen, Liang: 2 articles (05/2015 - 12/2011)|
|7.||Gao, Yaping: 2 articles (09/2014 - 05/2008)|
|8.||Liu, Yu: 2 articles (09/2014 - 05/2008)|
|9.||Yang, Guang: 2 articles (09/2014 - 05/2008)|
|10.||Kelley, William L: 2 articles (11/2010 - 09/2006)|
09/01/2014 - "Moreover, we found that RNAIII, the effector of agr system, was essential for the intracranial infection caused by S. "
02/01/2014 - "Furthermore, the sasX gene might be related to the expressions of PSMα and RNAIII and infection invasiveness."
01/15/2008 - "Furthermore, ST151 had elevated levels of RNAIII and cytolytic toxin-gene expression, consistent with the enhanced virulence observed during experimental infection. "
02/01/2004 - "aureus infection (RNAIII, hla and spa) and for the 16S rRNA. "
06/01/2001 - "As with RNAIII, the highest hla expression was detected in both strains early in infection. "
|3.||Septic Shock (Toxic Shock Syndrome)
11/01/2010 - "In the present study, we have examined the role of both SarA and RNAIII on the regulation of the promoter of tst, encoding staphylococcal superantigen toxic shock syndrome toxin 1 (TSST-1). "
02/01/2002 - "Expression of RNAIII, the effector molecule of the agr locus, was dramatically repressed in serum and in vivo, despite the increased expression of secreted virulence factors sufficient to cause toxic shock syndrome (TSS) in the animals. "
04/01/2004 - "This system down-regulates production of agr RNAIII, protein A, and toxic shock syndrome toxin 1 (TSST-1), particularly under low-oxygen conditions. "
09/01/2002 - "In experimental endocarditis, maximal RNAII activation in vegetations occurred early, followed by progressive increases in RNAIII activation (P<.05; 2 vs. 48 h); this paralleled significant increases in vegetation bacterial densities over time (P<.05; 2 and 6 vs. 48 h). "
09/01/2002 - "Activation and transcriptional interaction between agr RNAII and RNAIII in Staphylococcus aureus in vitro and in an experimental endocarditis model."
12/01/2011 - "aureus (MRSA) bloodstream isolates (5 agr-I [clonal complex 45, or CC45] and 5 agr-II [CC5]) were studied for (i) agr function, (ii) RNAIII transcriptional profiles, (iii) agr locus sequences, (iv) intrinsic virulence and responses to vancomycin therapy in an experimental infective endocarditis (IE) model, and (v) in vivo RNAIII expression. "
04/01/2004 - "Overexpression of SrrAB, which represses agr RNAIII, TSST-1, and protein A in vitro, decreases virulence in the rabbit endocarditis model. "
|2.||Virulence Factors (Pathogenicity Factors)
|4.||Biological Markers (Surrogate Marker)
|5.||Staphylococcal Protein A (A, Protein)
|10.||Staphylococcal enterotoxin F