Effects of human β-defensin-3 on biofilm formation‑regulating genes dltB and icaA in Staphylococcus aureus.

An understanding of the regulatory mechanisms that drive Staphylococcus aureus biofilm formation may lead to the development of an effective strategy to control the increasing number of refractory clinical infections it causes. The present study examined the effects of the antimicrobial agent human β‑defensin 3 (hBD‑3) and the antibiotics vancomycin and clindamycin on the expression of the S. aureus biofilm formation‑regulating genes, icaA and dltB, during bacterial adhesion and biofilm formation.

Debriding effect of bromelain on firearm wounds in pigs.

Background: Wound excision is the standard treatment for firearm wounds. However, achieving a satisfactory curative effect is difficult because of the traumatic mechanism of high-velocity projectiles. We propose a new therapy by using topical bromelain as a supplement to wound incision for the debridement of firearm wounds.

[Hepatitis B virus X protein regulates c-met promoter via the ERKs singal pathway in HepG2 cells].

Objective: To explore the signal pathway mediating the regulatory effect of Hepatitis B virus X protein (HBX) on c-met gene promoter in HepG2 cells.

Methods: The expression of c-met in HBX-transfected HepG2 cells treated with different signal pathway inhibitors was detected by western blot, the invasion capability of cells was determined by Matrigel invasion assay.

Results: ERK inhibitor U0126 inhibited the expression of the c-Met in HBx-transfected HepG2 cells.

[The effect of hepatitis B virus X protein on the c-met promoter activity in HepG2 cells].

Objective: To confirm the effect of hepatitis B virus X (HBx) protein on the c-met promoter activity in HepG2 cells.

Method: The expression of c-met protein was detected by western blot in HBx-transfected HepG2 cells, the human c-met promote activity was checked by luciferase assay using five different constructs with deletion or point mutation.

Results: HBx protein stimulated the expression of the c-met in HepG2 cells.