OBJECTIVETo research the relationship between the virulence factors of Saccharomyces albicans (S. albicans) and the random amplified polymorphic DNA (RAPD) bands of them, and establish the regression model by multiple regression analysis.

METHODSExtracellular phospholipase, secreted proteinase, ability to generate germ tubes and adhere to oral mucosal cells of 92 strains of S. albicans were measured in vitro; RAPD-polymerase chain reaction (RAPD-PCR) was used to get their bands. Multiple regression for virulence factors of S. albicans and RAPD-PCR bands was established.

RESULTSThe extracellular phospholipase activity was associated with 4 RAPD bands: 350, 450, 650 and 1 300 bp (P < 0.05); secreted proteinase activity of S. albicans was associated with 2 bands: 350 and 1 200 bp (P < 0.05); the ability of germ tube produce was associated with 2 bands: 400 and 550 bp (P < 0.05).

CONCLUSIONSome RAPD bands will reflect the virulence factors of S. albicans indirectly. These bands would contain some important messages for regulation of S. albicans virulence factors.

DNA ; Polymerase Chain Reaction ; Random Amplified Polymorphic DNA Technique ; Saccharomyces ; Virulence Factors

Staphylococcus utilizes vancomycin-resistance associated sensor/regulator ( VraSR) , a two-component signal transduction system ( TCS) , to sense and respond to cell wall damage and to adapt to environmental changes through regulating transcriptions of downstream genes. It has been indicated that VraSR can regulate the transcription of a series of genes involved in the synthesis of peptidoglycan, drug re-sistance, and virulence in Staphylococcus aureus ( S. aureus) . A similar two-component system, VraSR, is also present in Staphylococcus epidermidis ( S. epidermidis ) , sharing a high homology with the VraSR of S. aureus. Little is known about the functions of VraSR in S. epidermidis and it is not yet clear what the simi-larities and differences in resistance and pathogenicity are. Based on the previous work of our group, a brief review on the regulation mechanism of staphylococcal VraSR was performed.