Effects of diode laser setting for laryngeal surgery in a rabbit model.

PURPOSE: To study the damaging effect of different diode laser settings on vocal folds 7 days after injury in a rabbit model. METHODS: Twenty-one male New Zealand white rabbits were randomized into three groups with seven animals per group. A 980-nm diode laser was used to create a single spot injury in each vocal fold. Different modulation frequencies (10 Hz versus 1000 Hz) in pulsed mode, different powers (3 W versus 5 W), and distinct wave modes of radiation (pulsed versus continuous) were compared. RESULTS: The extent of the inflammatory infiltrate and ablation crater were greater when using 5-W optical power compared with 3 W. The extent and depth of the inflammatory infiltrate, and the width and depth of the ablation crater were greater with continuous wave mode compared with pulsed mode. The density of collagen fibers only increased when using the laser in continuous wave mode. CONCLUSION: The use of the 980-nm diode laser with an output power of 5 W produced an increased extent of thermal injury compared to an output power of 3 W and, more importantly, using continuous rather than pulsed wave mode significantly increased the extent and depth of thermal injury in rabbit vocal folds.

TREATMENT WITH HUMAN UMBILICAL CORD-DERIVED MESENCHYMAL STEM CELLS IN A PIG MODEL OF SEPSIS-INDUCED ACUTE KIDNEY INJURY: EFFECTS ON MICROVASCULAR ENDOTHELIAL CELLS AND TUBULAR CELLS IN THE KIDNEY.

ABSTRACT: Background: Approximately 50% of patients with sepsis develop acute kidney injury (AKI), which is predictive of poor outcomes, with mortality rates of up to 70%. The endothelium is a major target for treatments aimed at preventing the complications of sepsis. We hypothesized that human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) could attenuate tubular and endothelial injury in a porcine model of sepsis-induced AKI. Methods: Anesthetized pigs were induced to fecal peritonitis, resulting in septic shock, and were randomized to treatment with fluids, vasopressors, and antibiotics (sepsis group; n = 11) or to that same treatment plus infusion of 1 × 10 6 cells/kg of hUC-MSCs (sepsis+MSC group; n = 11). Results: At 24 h after sepsis induction, changes in serum creatinine and mean arterial pressure were comparable between the two groups, as was mortality. However, the sepsis+MSC group showed some significant differences in comparison with the sepsis group: lower fractional excretions of sodium and potassium; greater epithelial sodium channel protein expression; and lower protein expression of the Na-K-2Cl cotransporter and aquaporin 2 in the renal medulla. Expression of P-selectin, thrombomodulin, and vascular endothelial growth factor was significantly lower in the sepsis+MSC group than in the sepsis group, whereas that of Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) was lower in the former. Conclusion: Treatment with hUC-MSCs seems to protect endothelial and tubular cells in sepsis-induced AKI, possibly via the TLR4/NF-κB signaling pathway. Therefore, it might be an effective treatment for sepsis-induced AKI.