No abstract

Gas6 increases invasion of oral squamous cell carcinoma, and the invasion correlates with the increased AKT and the downregulation of pro-inflammatory cytokines. These results may prove useful in providing avenues that explain the role of Gas6 in the development and progression of oral squamous cell carcinoma.

No abstract

The development of the electronic cigarette (e‐cig) has given rise to a new, largely unregulated market within the smoking industry. Proponents suggest they assist with smoking cessation as e‐cigs rely on vapor produced by heating an e‐liquid to deliver flavored nicotine. While generally assumed to be less harmful than traditional tobacco cigarette smoke, knowledge about the toxicity of the e‐liquid consumed via such electronic devices is still scarce. During use of an electronic cigarette, the oral cavity and respiratory system receives direct exposure to the chemical constituents of the e‐liquids. An additional area of concern is the effect of e‐cigs on the placenta due to a potential misconception that e‐cigs are safer to use during gestation than classical tobacco. Traditional cigarette smoke compromises health by increasing inflammation, mediated through receptor for advanced glycation end‐products (RAGE) signaling. Pro‐inflammatory profiles have been suggested following e‐cig exposure; however, the role of RAGE in e‐cig liquid‐induced inflammation has not been resolved. The purpose of this study was to determine the effects of e‐liquid on RAGE expression and levels of several pro‐inflammatory cytokines mediated at least in part by RAGE signaling such as interleukin (IL)‐1b, IL‐6, IL‐8 and tumor necrosis factor (TNF)‐a. Gingival epithelium (Ca9‐22), pulmonary epithelium (A549), and placental trophoblast (BeWo) cells were exposed to 0, 2, or 4% of Cuttwood™ e‐cigarette liquid, a popular national brand, for 24 hours. Cytotoxicity was measured by LDH assays. E‐cig induced RAGE upregulation was confirmed by quantitative RT‐PCR in A549 and Ca9‐22 cells while only a trend in RAGE upregulation was observed in BeWo cells. QPCR revealed increased transcription of IL‐1b, IL‐6, IL‐8 and TNF‐a in each cell type. Finally, a multiplex cytokine array was performed in order to precisely determine the secretion of these and other pro‐inflammatory modulators. In an effort to block RAGE signaling, we have synthesized a family of anionic, partially lipophilic sulfated polysaccharide derivatives known as semi‐synthetic glycosaminoglycan ethers (SAGEs). Co‐treatment of e‐cig liquid and SAGEs resulted in amelioration of inflammatory cytokine secretion. Together, these results provide a new perspective on a possible mechanism whereby e‐cigarette inflammation occurs.Support or Funding InformationThis work was supported by a grant from the Flight Attendant's Medical Research Institute (FAMRI, PRR) and a BYU Mentoring Environment Grant (PRR).

active research into the development of ureteral stents with surface coatings and smoothing of the surface to reduce foreign body adhesion. In this study, the novel ureteral stent coated with polydopamine (PDA), which is formed by the polymerization of dopamine and close to the substances existed in human body and so has a low recognition reaction as a foreign substance, were investigated for ability to prevent crystal (Calcium: Ca) adhesion.METHODS: The ureteral stent was incubated in artificial urine at 37 C for 3 weeks, and the amount of Ca deposition on the surface of the ureteral stent was compared between the PDA-coated stent and commercially available stents by microscopic observation and Inductively Coupled Plasma (ICP) analysis. As to in vivo study, in rat model of hypercalciuria induced by drinking ethylene glycol and ammonium chloride, stents were implanted in the bladder for one month and Ca deposition on the surface of the ureteral stent was determined.RESULTS: After immersion in artificial urine for 3 weeks, the PDA-coated ureteral stent showed less Ca deposition on the stent surface than the commercially available ureteral stent (p[0.0468). There was no significant difference in the increase in pH of the artificial urine in which the ureteral stent was immersed between the PDA-coated and commercially available ureteral stents. With respect to the rat experimental model with Ca including-urine, the PDA-coated ureteral stent had less Ca deposition on the stent surface than the commercially available stent (p[0.0412). No apparent safety-related adverse events were observed.CONCLUSIONS: Our novel PDA-coated ureteral stent showed less amount of Ca deposition on the stent surface than commercial stents in artificial urine. The experimental rat model with Ca includingurine also showed a similar data of less Ca deposition on the stent surface than commercial stent, suggesting that this novel stent is less likely to cause stent occlusion (WO/2022/176834).