Interspecific differences in oxidative DNA damage after hydrogen peroxide exposure of sea urchin coelomocytes.

Interspecific comparison of DNA damage can provide information on the relative vulnerability of marine organisms to toxicants that induce oxidative genotoxicity. Hydrogen peroxide (H2O2) is an oxidative toxicant that causes DNA strand breaks and nucleotide oxidation and is used in multiple industries including Atlantic salmon aquaculture to treat infestations of ectoparasitic sea lice. H2O2 (up to 100 mM) can be released into the water after sea lice treatment, with potential consequences of exposure in nontarget marine organisms. The objective of the current study was to measure and compare differences in levels of H2O2-induced oxidative DNA damage in coelomocytes from Scottish sea urchins Echinus esculentus, Paracentrotus lividus, and Psammechinus miliaris. Coelomocytes were exposed to H2O2 (0-50 mM) for 10 min, cell concentration and viability were quantified, and DNA damage was measured by the fast micromethod, an alkaline unwinding DNA method, and the modified fast micromethod with nucleotide-specific enzymes. Cell viability was >92% in all exposures and did not differ from controls. Psammechinus miliaris coelomocytes had the highest oxidative DNA damage with 0.07 ± 0.01, 0.08 ± 0.01, and 0.07 ± 0.01 strand scission factors (mean ± SD) after incubation with phosphate-buffered saline, formamidopyrimidine-DNA glycosylase, and endonuclease-III, respectively, at 50 mM H2O2. Exposures to 0.5 mM H2O2 (100-fold dilution from recommended lice treatment concentration) induced oxidative DNA damage in all three species of sea urchins, suggesting interspecific differences in vulnerabilities to DNA damage and/or DNA repair mechanisms. Understanding impacts of environmental genotoxicants requires understanding species-specific susceptibilities to DNA damage, which can impact long-term stability in sea urchin populations in proximity to aquaculture farms.

Clinical significance of activated Wnt/ß-catenin signaling in apoptosis inhibition of oral cancer.

Wnt/ß-catenin signaling is an evolutionarily conserved pathway and plays a crucial role in regulating cancer cell proliferation and tumorigenesis. However, the molecular mechanism behind the Wnt/ß-catenin signaling-mediated carcinogenesis and apoptosis resistance in oral squamous cell carcinoma is not well characterized so far. In the present study, we have investigated the effect of ß-catenin depletion of the perversely activated Wnt/ß-catenin signaling pathway on apoptosis resistance and tumorigenesis of the human OSCC cell line SCC-55. RT-PCR and western blot analysis demonstrated that the Wnt/ß-catenin signaling pathway and its downstream targets such as DKK1 and AXIN2 are aberrantly activated in SCC-55 cells. Furthermore, upon silencing (RNA interference) of ß-catenin in SCC-55, cells became more sensitive toward the chemotherapeutic drugs and thus resulted in apoptotic cell death. Meanwhile, flow cytometry analysis confirmed the enhanced apoptosis and activation of caspases in ß-catenin RNAi cells. Besides ensuing ß-catenin-siRNA transfection, the cell proliferation and cancer colony generating efficiencies are significantly impeded compared to the non-transfected cells. Furthermore, the tumorigenicity was inhibited by the downregulation of OCT-4 in ß-catenin-silenced SCC-55 cells. Altogether, Wnt/ß-catenin signaling could potentially target anti-cancer drugs to induce apoptosis and achieve a better clinical outcome.

A retrospective study of 30,959 implants: Risk factors associated with early and late implant loss.

AIM: This retrospective study assessed the risk factors associated with early and late implant loss at the patient- and implant-based analysis. MATERIALS AND METHODS: A total of 18,199 patients received 30,959 dental implants during the years 2011-2015. Age, gender, jaw, location, implant brands, implant length and diameter, bone augmentation procedures, and the number of implants placed per patient were recorded. A multivariate generalized estimating equation (GEE) logistic regression was used to identify risk factors related to both early and late implant loss. RESULTS: The cumulative survival rates were 98.0% for patients and 98.7% for implants after 1-6 years observation time. A total of 183 patients with 194 implants were lost before or at the abutment connection, and 193 patients with 209 implants were lost after occlusal loading of the implant fixture. The multivariable GEE logistic regression showed that males, patients aged ≥41 years, and mandibular anterior location were risk factors for early implant loss. In the case of late implant loss, males, patients aged ≥41 years, bone augmentation and short implants were correlated with a significantly increased failure rate. CONCLUSIONS: General factors such as male sex, elderly patients, mandibular anterior location, bone augmentation and short implants were associated with implant loss.

[Extraarticular diffuse pigmented villonodular synovitis of the temporomandibular joint: report of one case and review of the literature].

Diffuse pigmented villonodular synovitis (PVNS) in the temporomandibular joint (TMJ) is distinctly rare. This article reported a case of extra-articular type of PVNS of the TMJ, and reviewed the previously reported cases in the literature. It is concluded that PVNS can be diagnosed by characteristic MRI finding, wide local excision including a total synovectomy and postoperative radiotherapy should be adopted.