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1.
J Gambl Stud ; 2024 Aug 28.
Artículo en Inglés | MEDLINE | ID: mdl-39196468

RESUMEN

This study examined the relationships between marketing exposure, in-game purchase, problem gaming, online simulated gambling game playing, and psychological distress. Data were obtained from a sample of 2,595 seventh-grade students from 30 middle schools in Taiwan. A self-administered questionnaire was conducted in 2020. The results indicated that 94% of adolescents engage in online gaming, with 38% making in-game purchases, and 9% playing online simulated gambling games. The multiple regression results showed that adolescents who are exposed to higher levels of gaming marketing, influenced by advertising effects, involved in in-game purchases, and have lower levels of active parental mediation were more likely to experience problem gaming. Adolescents who have increased exposure to gambling game marketing, are influenced by advertising effects, are involved in in-game purchases, and who are experiencing problem gaming were more likely to engage in online simulated gambling game playing and token purchasing. Involvement in in-game purchases, problem gaming, and playing online simulated gambling games were associated with higher levels of psychological distress and poor sleep quality. In conclusion, the results of this study link adolescents' exposure to marketing with their involvement in in-game purchases, problem gaming, and engaging in online simulated gambling.

2.
Int J Nanomedicine ; 19: 10435-10453, 2024.
Artículo en Inglés | MEDLINE | ID: mdl-39430308

RESUMEN

Introduction: Cisplatin is one of the most effective chemotherapeutic drugs used in oral cancer treatment, but systemic administration has side effects. The purpose of this study was to evaluate the effect of iontophoresis on the enhancement of cisplatin release from cisplatin-encapsulated chitosan nanoparticles. Methods: The effect of different mass ratios of chitosan to tripolyphosphate (TPP) (5:1, 10:1, 15:1, 20:1) on the encapsulation efficiency of cisplatin was investigated. Uptake of cisplatin-encapsulated chitosan by cells was observed using a confocal laser scanning microscope. The cell viability at different cisplatin concentrations was examined using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Three iontophoresis methods, namely constant-current chronopotentiometry (CCCP), cyclic chronopotentiometry (CCP), and differential pulse voltammetry (DPV), were used to enhance cisplatin release from cisplatin-encapsulated chitosan nanoparticles. In addition, mouse oral squamous cell carcinoma cell lines were implanted into the mouse oral mucosa to induce oral cancer. The effects of enhanced cisplatin release by CCCP, CCP, and DPV on tumor suppression in mice were evaluated. Tumors and lymph nodes were isolated for hematoxylin-eosin staining and immunohistochemistry staining including Ki-67 and pan CK after sacrifice. Inductively coupled plasma mass spectrometry was conducted to quantify the platinum content within the tumors. Results: The results showed that nanoparticles with a mass ratio of 15:1 exhibited the highest cisplatin encapsulation efficiency (approximately 15.6%) and longest continued release (up to 35 days) in phosphate buffered saline with a release rate of 100%. Cellular uptake results suggested that chitosan nanoparticles were delivered to the cytoplasm via endocytosis. The results of the MTT assay revealed that the survival rate of cells decreased as the cisplatin concentration increased. The CCP (1 mA, on:off = 1 s: 1 s) and DPV (0-0.06 V) groups were the most effective in inhibiting tumor growth, and both groups exhibited the lowest percentage of Ki-67 positive and pan CK positive. Conclusion: This study is the first to investigate and determine the efficacy of DPV in enhancing in vivo drug release from nanoparticles for the treatment of cancer in animals. The results suggest that the CCP and DPV methods have the potential to be combined with surgery for oral cancer treatment.


Asunto(s)
Antineoplásicos , Quitosano , Cisplatino , Iontoforesis , Neoplasias de la Boca , Nanopartículas , Quitosano/química , Animales , Cisplatino/farmacocinética , Cisplatino/farmacología , Cisplatino/química , Cisplatino/administración & dosificación , Neoplasias de la Boca/tratamiento farmacológico , Neoplasias de la Boca/patología , Línea Celular Tumoral , Antineoplásicos/farmacocinética , Antineoplásicos/química , Antineoplásicos/farmacología , Antineoplásicos/administración & dosificación , Ratones , Nanopartículas/química , Iontoforesis/métodos , Supervivencia Celular/efectos de los fármacos , Mucosa Bucal/efectos de los fármacos , Mucosa Bucal/metabolismo , Carcinoma de Células Escamosas/tratamiento farmacológico , Carcinoma de Células Escamosas/patología , Liberación de Fármacos , Humanos , Portadores de Fármacos/química , Portadores de Fármacos/farmacocinética , Modelos Animales de Enfermedad , Polifosfatos
3.
J Dent Sci ; 19(3): 1434-1442, 2024 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-39035337

RESUMEN

Background/purpose: Periodontitis is associated with various systemic diseases, potentially facilitated by the passage of Porphyromonas gingivalis outer membrane vesicles (Pg-OMVs). Several recent studies have suggested a connection between Pg-OMVs and neuroinflammation and neurodegeneration, but the precise causal relationship remains unclear. This study aimed to investigate the mechanisms underlying these associations using in vitro models. Materials and methods: Isolated Pg-OMVs were characterized by morphology, size, and gingipain activity. We exposed SH-SY5Y neuroblastoma cells and BV-2 microglial cells to various concentrations of Pg-OMVs. Cell morphology, a 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, an enzyme-linked immunosorbent assay, and Western blot analysis were used to evaluate the cellular mechanism underlying Pg-OMV-induced neurotoxicity in neuronal cells and inflammatory responses in microglial cells. Results: Exposure to Pg-OMVs induced neurotoxicity in SH-SY5Y cells, as evidenced by cellular shrinkage, reduced viability, activation of apoptotic pathways, and diminished neuronal differentiation markers. Gingipain inhibition mitigated these effects, suggesting that gingipain mediates Pg-OMVs-induced neurotoxicity in SH-SY5Y cells. Our research on neuroinflammation suggests that upon endocytosis of Pg-OMVs by BV-2 cells, lipopolysaccharide (LPS) can modulate the production of inducible nitric oxide synthase and tumor necrosis factor-alpha by activating pathways that involve phosphorylated AKT and the phosphorylated JNK pathway. Conclusion: Our study demonstrated that following the endocytosis of Pg-OMVs, gingipain can induce neurotoxicity in SH-SY5Y cells. Furthermore, the Pg-OMVs-associated LPS can trigger neuroinflammation via AKT and JNK signaling pathways in BV-2 cells.

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