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2.
J Affect Disord ; 362: 877-884, 2024 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-39009310

RESUMO

BACKGROUND: The issue of problematic Internet use (PIU) amongst college students is emerging as a major concern for mental health. Factors such as health literacy, subjective well-being and the extent of social support may be critical in preventing PIU. However, the complex relationship between these factors has not been extensively explored in research. METHODS: A national cross-sectional study based on multistage random sampling was conducted in China in 2022. The subjects for this study were 7669 college students who completed a set of questionnaires assessing their health literacy, subjective well-being, PIU and social support. A structural equation model (SEM) was utilised for exploring the mediating effect of subjective well-being, and the PROCESS macro was used to test the moderating effect of social support. RESULTS: After controlling for demographic factors, a significantly negative correlation was found between health literacy and PIU, and subjective well-being partially mediated this relationship. In addition, social support was negatively related to PIU and could moderate the relationship between health literacy and subjective well-being and between subjective well-being and PIU. LIMITATIONS: This is a cross-sectional study, and the results cannot inform the causality between these variables. CONCLUSION: Results revealed that the relationship between health literacy and PIU was partially mediated by subjective well-being in college students. The correlation between health literacy and subjective well-being and between subjective well-being and PIU were moderated by social support. Thus, future interventions for college students' PIU should be facilitated by improving health literacy, subjective well-being and social support.


Assuntos
Letramento em Saúde , Apoio Social , Estudantes , Humanos , Letramento em Saúde/estatística & dados numéricos , Masculino , Feminino , Estudantes/psicologia , Estudantes/estatística & dados numéricos , Estudos Transversais , China , Adulto Jovem , Universidades , Inquéritos e Questionários , Adulto , Adolescente , Transtorno de Adição à Internet/psicologia , Saúde Mental , Satisfação Pessoal
3.
QJM ; 2024 Jul 30.
Artigo em Inglês | MEDLINE | ID: mdl-39078203
5.
Cardiovasc Diagn Ther ; 14(1): 223-225, 2024 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-38434563
8.
Korean J Physiol Pharmacol ; 27(4): 345-356, 2023 Jul 01.
Artigo em Inglês | MEDLINE | ID: mdl-37386832

RESUMO

This study aimed to assess the effects of exogenous hydrogen sulfide (H2S) on abdominal aorta coarctation (AAC) induced myocardial fibrosis (MF) and autophagy in rats. Forty-four Sprague-Dawley rats were randomly divided into control group, AAC group, AAC + H2S group, and H2S control group. After a model of rats with AAC was built surgically, AAC + H2S group and H2S group were injected intraperitoneally with H2S (100 µmol/kg) daily. The rats in the control group and the AAC group were injected with the same amount of PBS. We observed that H2S can improve left ventricular function and the deposition of myocardial collagen fibers, inhibit pyroptosis, down-regulate the expression of P-eif2α in myocardial tissue, and inhibit cell autophagy by activating the phosphatidylinositol 3-kinase (PI3K)/AKT1 signaling pathway (p < 0.05). In addition, angiotensin II (1 µM) H9c2 cardiomyocytes were injured in vitro experiments, and it was also observed that pyroptosis was inhibited after H2S (400 µmol/kg) intervention, the expression of P-eif2α in cardiomyocytes was significantly down-regulated, and the PI3K/AKT1 signaling pathway was activated at the same time. Therefore, increasing the expression of P-eif2α reverses the activation of the PI3K/AKT1 signaling pathway by H2S. In conclusion, these findings suggest that exogenous H2S can ameliorate MF in rats with AAC by inhibiting pyroptosis, and the mechanism may be associated with inhibiting the phosphorylation of eif2α and activating the PI3K/AKT1 signaling pathway to inhibit excessive cell autophagy.

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