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1.
J Adv Nurs ; 75(5): 1010-1017, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30375059

RESUMO

AIMS: To explore the effectiveness of an oral hygiene programme combined with home phone counselling on hepatitis C patients during antiviral treatment. BACKGROUND: Hepatitis C virus infection is the leading cause of liver diseases. Evidence indicates that the antiviral treatment for hepatitis C virus infection has been successful, albeit its many side effects, such as discomfort symptoms of oral ulcers, which, in turn, leads to discontinued treatment. Inappropriate oral hygiene may worsen the side effects and increase the risk of dropping out of the treatment. DESIGN: A quasi-experimental pre-post-test design was used. METHODS: The oral hygiene programme was based on a standardized protocol of oral health care combined with home phone counselling. The participants were recruited from an outpatient clinic between August 2016 and July 2017. The generalized estimating equation was used for repeated measures of oral health behaviour, oral health status and discomfort symptoms. FINDINGS: Thirty-four participants completed this study. The findings indicated that the oral hygiene programme significantly improved tooth brushing, use of dental floss and oral comfort. The result showed that the participants' oral health status significantly improved in 3 months. CONCLUSIONS: This pilot study supports the finding that an oral hygiene programme can reduce oral discomfort, improve oral hygiene behaviour, and enhance the oral health status of hepatitis C patients receiving treatment. This is a simple and low-cost programme, which can be performed at home easily and boosts the completion of antiviral treatment.


Assuntos
Antivirais/uso terapêutico , Aconselhamento/métodos , Promoção da Saúde/métodos , Hepatite C/tratamento farmacológico , Higiene Bucal/educação , Telemedicina/métodos , Telefone , Adulto , Idoso , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Projetos Piloto , Taiwan , Adulto Jovem
2.
Arch Biochem Biophys ; 622: 26-35, 2017 05 15.
Artigo em Inglês | MEDLINE | ID: mdl-28442401

RESUMO

TRIB3, which is a pseudokinase known to regulate multiple pro-survival pathways, appears to be a potential therapeutic target for the treatment of human tumors. However, its precise role in cancer is controversial, as TRIB3 protein levels have been associated with both good and poor prognosis in cancer patients. Here, we investigated the significance of TRIB3 expression in the survival of gastric cancer cells exposed to anticancer drugs. We found that the tested anticancer drug, doxorubicin, induced cytotoxicity by decreasing TRIB3 transcription, which was followed by apoptotic cell death. Moreover, TRIB3 siRNA knockdown appeared to enhance doxorubicin-induced apoptosis in gastric cancer cells, concurrently with altering the expression of downstream apoptotic factors. Conversely, overexpression of TRIB3 significantly protected cells against doxorubicin-induced apoptosis. Our results indicate that downregulation of TRIB3 appears to promote cell death and enhance doxorubicin-induced apoptosis, supporting the anti-apoptotic role of TRIB3. The inductions of three classes of MAPKs failed to affect doxorubicin-mediated TRIB3 downregulation, while TRIB3 overexpression did not affect doxorubicin-induced MAPK activation. In sum, our findings indicate that TRIB3 plays an anti-apoptotic role in doxorubicin-treated gastric cancer cell lines, perhaps indicating that the status of TRIB3 expression in response to anticancer drugs, such as doxorubicin, irinotecan or oxaliplatin, may reflect the efficiency for cancer therapy.


Assuntos
Antibióticos Antineoplásicos/farmacologia , Proteínas de Ciclo Celular/genética , Regulação para Baixo/efeitos dos fármacos , Doxorrubicina/farmacologia , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Proteínas Serina-Treonina Quinases/antagonistas & inibidores , Proteínas Repressoras/genética , Neoplasias Gástricas/tratamento farmacológico , Neoplasias Gástricas/genética , Apoptose/efeitos dos fármacos , Linhagem Celular Tumoral , Mucosa Gástrica/metabolismo , Humanos , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Proteínas Serina-Treonina Quinases/genética , Estômago/efeitos dos fármacos , Estômago/patologia , Neoplasias Gástricas/metabolismo , Neoplasias Gástricas/patologia
3.
Cancer Manag Res ; 10: 4237-4248, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-30323679

RESUMO

BACKGROUND: Capsaicin (8-methyl-N-vanillyl-6-nonenamide) is one of the main pungent components of chili peppers and has been shown to exert various effects on numerous physiological processes. Recent studies have focused on the chemopreventive effects of capsaicin, which can combat growth in various human cancer cell systems. The tribbles-related protein 3 (TRIB3) is evolutionarily conserved from Drosophila to humans. In the latter, TRIB3 is a key determinant in numerous cellular processes, including apoptosis. PURPOSE: The aim of this study was to examine the importance of TRIB3 in the antitumor efficacy of capsaicin in human cancer cells, and further assess potential mechanism(s) underlying the capsaicin-induced upregulation of TRIB3. METHODS: Human cancer cell lines were treated with capsaicin, then evaluated for levels of TRIB3 and molecules related to apoptosis or signaling pathways. The impact of TRIB3 on capsaicin-induced apoptosis was investigated using si-RNA or overexpression of TRIB3. RESULTS: It is the first time to show that TRIB3 is targeted by capsaicin to promote apoptosis. Capsaicin promotes apoptotic cell death by upregulating TRIB3 expression in cancer cells. Overexpression of TRIB3 enhances capsaicin-induced apoptosis, and TRIB3 knockdown experiments demonstrate that the effect of capsaicin in apoptotic cell death is correlated with the induction of TRIB3 in cancer cells. Finally, enhancements in gene expression and protein stability are involved in the capsaicin-induced upregulation of TRIB3. CONCLUSION: Our results show that the capsaicin-induced upregulation of TRIB3 triggers apoptosis and thereby contributes to the suppression of cell growth in cancer cell lines.

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