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The Evolution of KTP Laser Vaporization of the Prostate
Petros Sountoulides,Peter Tsakiris 연세대학교의과대학 2008 Yonsei medical journal Vol.49 No.2
The search for a minimally invasive approach to the treatment of Lower Urinary Tract Symptoms (LUTS) suggestive of Benign Prostatic Hyperplasia (BPH) is probably as old as Transurethral Resection of the Prostate (TURP). In an effort to overcome the limitations and morbidities of TURP, and in light of evidence suggesting that medical treatment for BPH has a limited life-span, laser-based treatments have emerged during the last decade. Photoselective Vaporization of the Prostate (PVP) by the “GreenLight” KTP laser is considered one of the most promising options, one that is constantly evolving new technologies in prostate surgery. In this overview of KTP laser usage in BPH treatment, we will briefly discuss the evolution of this modality since it was first introduced and focus on the available evidence regarding safety, efficacy and cost parameters of its application.
Reactive Oxygen Species Modulate Nitric Oxide-mediated Cytotoxicity in Osteoblasts
Damoulis, Petros D.,Hauschka, Peter V. Korean Academy of Oral Biology and the UCLA Dental 1997 International Journal of Oral Biology Vol.22 No.2
Nitric oxide (NO), a free radical produced enzymatically through the L-arginine/NO synthase (NOS) pathway, has been shown to cause apoptotic cell death in osteoblasts when present at high concentrations. Loss of osteoblast viability could be a potentially important factor during inflammatory bone loss. Post-confluent MC3T3-E1 mouse clonal osteogenic cells were cultured under high NO conditions in the presence of reactive oxygen species (ROS) scavengers. The superoxide scavengers, superoxide dismutase (SOD) and TEMPOL, increased cytokine-mediated cytotoxicity in osteoblasts, and they dramatically enhanced SNAP-mediated cell death. On the other hand, catalase, a hydrogen peroxide scavenger, protected the cells from cytokine toxicity, whereas it showed no effect on osteoblast survival after SNAP treatment. Interestingly, catalase also abolished cytokine-induced nitrite production, possibly by inhibiting the inducible NOS. Simultaneous inhibition of NO and superoxide in cytokine-stimulated MC3T3-E1 inhibited lytic cell death when compared to NO inhibition alone, but such treatment also increased loss of viable cells, possibly by increasing the available free NO which induced apoptosis. These results indicate that osteoblasts produce ROS which can react with nitric oxide, and implicate NO as the primary mediator of cytokine toxicity. It is suggested that the mechanism of these interactions should be further clarified so that the potential of free radical-targeted treatment of inflammatory bone diseases could be subsequently explored.