Background/Aims: Leupaxin (LPXN) is a member of the paxillin protein family. Several studies have reported that LPXN regulates cancer development; however, the role of LPXN in bladder cancer remains unknown. Methods: The expression of LPXN in bladder cancer cells and tissues was determined by real-time PCR, western blotting, and immunohistochemistry, respectively. The biological role of LPXN in bladder cancer cell proliferation, invasion, and angiogenesis was explored both in vitro and in vivo. Results: LPXN expression was elevated in bladder cancer tissues and cell lines compared to adjacent non-tumor tissues and normal urothelial cells. High LPXN expression was correlated with large tumor size, advanced tumor stage, and poor survival in bladder cancer patients. Overexpression of LPXN significantly promoted the proliferation, invasion, and angiogenesis of bladder cancer cells, while suppressing LPXN had the opposite effects. The impact on tumor progression was abolished by inhibiting PI3K/ AKT signaling pathway. We further demonstrated that LPXN probably up-regulated S100P via the PI3K/AKT pathway. Conclusions: LPXN may facilitate bladder cancer progression by upregulating the expression of S100P via PI3K/AKT pathway. These results provide a novel insight into the role of LPXN in tumorigenesis and progression of bladder cancer and potential therapeutic target of bladder cancer.
BackgroundVolatile organic compounds (VOCs) are a large group of chemicals widely used in people's daily routines. Increasing evidence revealed the VOCs' accumulating toxicity. However, the VOCs toxicity in male prostate has not been reported previously. Thus, we comprehensively evaluated the association between VOCs and prostate-specific antigen (PSA).MethodsA total of 2016 subjects were included in our study from the National Health and Nutrition Examination Survey with VOCs, PSA, and other variables among U.S. average population. We constructed XGBoost Algorithm Model, Regression Model, and Generalized linear Model (GAM) to analyze the potential association. Stratified analysis was used to identify high-risk populations.ResultsXGBoost Algorithm model identified blood chloroform as the most critical variable in the PSA concentration. Regression analysis suggested that blood chloroform was a positive association with PSA, which showed that environmental chloroform exposure is an independent risk factor that may cause prostate gland changes [β, (95% CI), P = 0.007, (0.003, 0.011), 0.00019]. GAM observed the linear relationship between blood chloroform and PSA concentration. Meanwhile, blood chloroform linear correlated with water chloroform in the lower dose range, indicating that the absorption of water may be the primary origin of chloroform. Stratified associations analysis identified the high-risk group on the chloroform exposures.ConclusionThis study revealed that blood chloroform was positively and independently associated with total PSA level, suggesting that long-term environmental chloroform exposure may cause changes in the prostate gland.
Aim
To determine the efficacy of endodontic microsurgery for teeth with an undeveloped root apex and periapical periodontitis caused by an abnormal central cusp fracture after failed nonsurgical treatment.
Methodology
Eighty teeth in 78 patients were subjected to endodontic microsurgery. All patients were clinically and radiologically examined 1 year postoperatively. The data were statistically analyzed using SPSS 27.0 software.
Results
Of the 80 teeth in 78 patients, periapical lesions had disappeared in 77 teeth at 1-year postoperative follow-up, with a success rate of approximately 96.3% (77/80). The efficacy of endodontic microsurgery was not affected by sex, age, extent of periapical lesions, and presence of the sinus tract. Between-group differences were not statistically significant (P > 0.05).
Conclusions
Endodontic microsurgery can be an effective alternative treatment option for teeth with an undeveloped root apex and periapical periodontitis caused by an abnormal central cusp fracture after nonsurgical treatment failure.
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