The involvement of ataxia-telangiectasia mutated protein activation in nucleotide excision repair-facilitated cell survival with cisplatin treatment.

DNA damage can lead to either DNA repair with cell survival or to apoptotic cell death. Although the biochemical processes underlying DNA repair and apoptosis have been extensively studied, the mechanisms by which cells determine whether the damage will be repaired or the apoptotic pathway will be activated is largely unknown. We have studied the role of nucleotide excision repair (NER) in cisplatin DNA damage-induced apoptotic cell death using both normal human fibroblasts and NER-defective xeroderma pigmentosum (XP) XPA and XPG cells.

The initiative role of XPC protein in cisplatin DNA damaging treatment-mediated cell cycle regulation.

XPC is an important DNA damage recognition protein involved in DNA nucleotide excision repair. We have studied the role of the XPC protein in cisplatin treatment-mediated cell cycle regulation. Through the comparison of microarray data obtained from human normal fibroblasts and two individual XPC-defective cell lines, 486 genes were identified as XPC-responsive genes in the cisplatin treatment (with a minimal 1.

Volume and surface area study of tobramycin-polymethylmethacrylate beads.

Polymethylmethacrylate bone cement beads impregnated with antibiotic are a common treatment for patients with persistent articular joint infections or osteomyelitis. They also are used as a prophylaxis for infection in patients with large soft tissue wounds. The current study was designed to evaluate the relationship between bead geometry and elution of the antibiotic tobramycin by methodically varying the shape of the beads for a given set of volumes.